Hypertension – 1

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This is so common it’s a) almost insulting to write about; and b) absolutely necessary to appreciate & master all its subtle aspects.  Management can be easy, since there are so many meds to choose among.  But some patients’ pressures remain recalcitrant on even 5 or 6 together.  As such, we will (as usual) conveniently ignore treatment, and address diagnosis alone:

  1. How do we say a patient has Arterial Hypertension (HTN)
  2. Identifying the rare <1% of patients with “Secondary Hypertension” (i.e. due to another disease, vs. the omnipresent “essential” variety

Hopefully the depth of our discussion won’t seem too absurd; anyone who ever views a blood pressure should have some appreciation of what it all means.


Hypertension (HTN) = B/P > 140/90.  This correlates with cardiovascular sequelae.  Some patients might [???] warrant lower targets:

  • Diabetics were supposed to keep B/P’s <130/80, but now studies have found that using 140/90 was as good as anything.
  • Chronic Kidney Disease patients should have B/P’s <130/80; however, systolics <120 may increase stroke risk [i.e. don’t be too aggressive]
  • Patients with known cardiovascular disease: some trials show benefit in keeping systolics <135 instead of 140, others not.

Then there’s “Pre-Hypertension,” i.e. B/P’s >120/80.  This includes practically 40% of the population.  Treating “pre-hypertension” for a short time doesn’t seem to prevent ultimate development of sustained HTN.  Personally, I shirk from applying disease labels to people unless I’m convinced of bona fide benefit.  After all, if we worry about “Pre-Hypertension,” what about “Pre-Pre-Hypertension”?

So I personally aim for 140/90.  I’d like my renal failure patients a little lower, but certainly wouldn’t add a new med just because their systolic hit 134 one day.  All these numbers revolve around relative risk reduction in large populations; nit-picking may mean very little for an individual person.

So much for definition (i.e. target B/P goal).

Taking the Blood Pressure

Should we use automatic cuffs or manual ones?  The former are quick and ubiquitous, and validated in studies.  But you can’t imagine how many times I recheck the machine’s reading, & get something way different.  Once a medical assistant came to me with a critical value “115/113” [!!!].  I have no idea what happened (the manual repeat was in fact normal [duh]).

So for patients I’m managing for HTN, or for new diagnoses, I take it myself manually.

I tell patients that I believe in my own [expensive] stethoscope over a machine, but disclose that whoever makes the thing would probably trust their product more than a wall sphygomanometer plus somebody’s aged ears.

To take a manual pressure, inflate up to 200 & deflate slowly, or you’ll miss high systolics.  We use the disappearance of sounds as diastolic.  Still, note when sounds muffle, because that’s the diastolic in cases when they remain audible for more than 10 points more.  Points?  Notches?  We’re supposed to say “mm Hg,” even if mercury sphygmomanometers are unfortunately prohibited today [I do still use the term, if not the element].

Some common confounders that mess up B/P measurements:

  • Arm is too high (B/P false low) or hanging too low (B/P false high).  The brachial artery should be at heart level.
  • Cuff too big (false low) or too small (false high).  The cuff’s air bladder should wrap about 80% around the upper arm.
  • Arrhythmias confound machines.
  • Recent cigarette (within 30 min.) gives a false high.
  • Recent meal might give false high.
  • Cold room <54° F gives a false high [undressed in an ER???]
  • Pt talking during measurement can increase B/P 10 mmHg
  • Sympathomimetics (e.g. decongestants) can raise B/P (& rarely cause strokes)

Pain can obviously raise blood pressure.  One HIV patient who presented with severe neuropathy had B/P’s persistently >160/100; they completely normalized with symptom control.

I’ve seen frequent patients instinctively clench their fists when I attach the cuff, as if for a blood draw.  That can increase the systolic by 10 mmHg.

My doc once announced she would leave the room for 5 min., return & take my B/P without exchanging words.  That’s how they did it in Framingham.  So I sat waiting, wondering what my B/P was doing in the meantime, & betting that Framingham didn’t artificially interrupt a clinic visit.

Diagnosing “Hypertension”

The gold standard is a B/P >135/85 by ambulatory B/P monitoring.  This is unfortunately very hard to access in the U.S., if not impossible.  An alternative is to use home machines, averaging at least 12 different measurements.  But they may cost $80, & one 1998 German study that secretly compared machine memory with patient logs found major disagreements.

So we’re essentially left with using office measurements; besides, these are the basis of studies that find increased cardiovascular risk.  Recommendation is to require 3 separate readings, each at least a week apart.  My personal preference is consecutive readings, lest somebody who likes to label scours the chart for 3 values.  Or if not consecutive, I want 5 or 6 values for “Mild HTN”.  Of course, if the B/P is >180/110, or there’s end organ damage, we diagnose lots sooner.

This isn’t so hard in terms of initial diagnosis.  But what happens when your well-controlled patient comes in with an elevated reading?  Do we immediately step-up therapy?  Recheck a bunch more times?  Suggest supermarket machines (I never trust their quality control)?  We noted that home measurement reports may not be reliable; however, there’s also the concept of “therapeutic inertia,” i.e. the clinician doesn’t move despite abnormal values.

Bottom Line  —

  • Take the B/P however you do, watching out for external confounders
  • Require several elevated readings before making a diagnosis
  • Step-up therapy whenever it seems appropriate


Once we diagnose “HTN,” we perform an H&P and order a number of tests.  These serve several purposes, to identify:

  • Co-morbidities (e.g. fasting lipids & glucose)
  • End-organ damage of HTN itself (e.g. EKG, U/A for proteinuria, query for subtle exertional Sx of coronary artery disease)
  • Secondary causes of HTN

The last category is what’s relevant to our current topic [it’s always nice to be clear to ourselves why we do things, isn’t it?].  There are certain tests we do on everybody, reserving others for specific circumstances, and those with severe or recalcitrant HTN.

Over 99% of people with HTN have “Essential HTN,” which essentially means, nobody knows why.  Thus major work-ups are rarely indicated; but we don’t want to miss that special case.

Causes of Secondary Hypertension and Diagnostic Tests

  • Hypo- / Hyperthyroidism  →  TSH
  • Renal Disease  →   Creatinine; Proteinuria; Renal Ultrasound
  • 1° Aldosteronism  →   Ratio of plasma Aldosterone-to-Renin Activity
  • Medications (contraceptives, NSAIDs, antidepressants)  →  History
  • Alcoholism  →   History
  • Hyperparathyroidism  →  Serum calcium (and albumin)
  • Pheochromocytoma → 24° Urine (Catecholamines, Metanephrines)
  • Cushing’s Syndrome  →  24 hr. Urine for Cortisol
  • Obstructive Sleep Apnea  →  Polysomnogram
  • Renal Artery Stenosis  →  Duplex Ultrasound; MR / CT Angiogram
  • Aortic Insufficiency  →  Cardiac auscultation; Echocardiogram
  • Coarctation of Aorta  →  Echocardiogram; MR / CT Angiogram

 This table does not imply that we obtain all these tests on everyone.  Quite to the contrary, we rarely order the vast majority of them.  History & Physical Exam give us the necessary clues; we’ll explore all this in depth next posting.

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