What it Looks Like: Jugular Vein Distention

October 17, 2011 by 32 Comments

See also what Agonal Respirations, Seizures, and Cardiac Arrest and CPR look like

Jugular vein distention or JVD (alternately JVP — jugular vein pressure or jugular vein pulsation) is right up there among the most mentioned but least described clinical phenomena in EMS. If you tried to count how many times it occurs in your textbook, you’d run out of fingers, but many of us graduate without ever seeing so much as a picture of it, never mind developing the acumen to reliably recognize it in an emergency.

JVD is simply the visible “bulging” of the external jugular veins on either side of the neck. These are large veins that drain blood from the head and return it directly to the heart. Since they’re located near the surface, they provide a reasonably good measure of systemic venous pressure.

JVD is elevated any time venous return is greater than the heart’s ability to pump the blood back out. Remember that we’re not talking about the vessels that plug into the left heart; that involves the pulmonary arteries and veins, which are not visible in the neck. (Instead, the best indicator of pulmonary hypertension is audible fluid in the lungs.) Rather, we’re talking about the systemic vasculature, which drains into the right ventricle via the right atrium. When veins aren’t getting emptied, we look downstream to discover what portion of the pump is failing. JVD is therefore caused by right heart failure. (Of course, the most common cause of right heart failure is left heart failure, so that doesn’t mean it’s an isolated event.) If JVD isn’t the heart’s fault, then we look to fluid levels. Too much circulating volume will lead to bulging veins for obvious reasons; the flexible tubes are simply extra full.

Although it’s probably most often seen, and most diagnostic, in volume-overloaded CHF patients, the main reason JVD is harped upon in EMS is because it’s a useful sign of several acute emergencies. Mainly, these are obstructive cardiac conditions, where some sort of pressure is impeding the heart’s ability to expand, and immediate care to relieve the pressure is needed in order to prevent incurable deadness. Much like the bladder, the heart is just a supple bag of squishy muscle, and although muscle is very good at squeezing, it has no ability to actively expand. The heart therefore fills only with whatever blood passively flows into it, and if it’s being externally squeezed by pressure in the chest, it can’t fill very much.

Tension pneumothorax is perhaps the most common cause, where air leaks from the lungs into the chest cavity with no way to escape; as the pressure in the chest increases, it bears down on the heart. Associated symptoms are respiratory difficulty, decreased breath sounds on the affected side, and hypotension. Pneumothorax can be readily corrected by paramedics using needle decompression.

Cardiac tamponade is another cause, where fluid leaks from the heart into the pericardium, an inflexible sac that surrounds it (this leakage is called a pericardial effusion), eventually filling the available space and compressing the myocardium. Associated symptoms are hypotension and muffled heart sounds (these plus JVD are known as Beck’s triad). Tamponade cannot be treated in the field, but an emergency department can perform a pericardiocentesis, where a needle is inserted through the pericardium. (For the medics out there, electrical alternans on the monitor is also supportive of tamponade.)

A rather less common syndrome that can produce similar obstructive effects is severe constrictive pericarditis, inflammation of the pericardium usually caused by infection.

JVD is not an all-or-nothing finding — the amount of distention visible at the neck will depend on the degree of venous pressure. Gravity wants to pull blood back down, so the more venous pressure, the higher on the neck distention will climb; profound JVD reaches many inches up the neck, slight JVD will only cover a few centimeters. The pressure can actually be quantified by measuring the vertical height of the highest point of distention (measured from the heart itself, using the angle of Louis as a landmark), but this is probably more detail than is needed in the field. Suffice to say that distention reaching more than 2-4cm of vertical distance (as opposed to the distance on the neck) above the chest is usually considered pathological, and less than 1-2cm can be considered suggestive of hypovolemia.

If it changes with respiration, JVD should rise during expiration and fall with inspiration. Breathing in involves using your diaphragm to create “suction” in the chest, reducing pressure and allowing greater venous return — draining the jugulars. A paradoxical rise in JVD during inspiration (think: up when the chest goes up) is known as Kussmaul’s sign (not to be confused with Kussmaul respirations, which is a pattern of breathing), and is particularly suggestive of obstructive pathologies.

JVD can be difficult to appreciate in all but the most significant cases. It helps to turn the patient’s head away and illuminate the area with angled backlighting, which creates a “shadow” effect. Jugular pulsation should not be confused with a visibly bounding carotid pulse. To distinguish them, remember that although jugular veins may visibly pulsate, their rhythm is generally complex, with multiple pulsations for each single heartbeat (you can feel the carotid to compare the two). The jugular “pulse” will also never be palpable; the distention can be easily occluded by the fingers and will feel like nothing.

Strictly speaking, the internal jugular is usually considered more diagnostically useful than the external jugular, but it’s far harder to examine, so the latter is often used. For various reasons, many people also find the right jugular more useful than the left, although in an ambulance it’s harder to examine.

Most often, JVD is examined in an inclined or semi-Fowler’s position of 30-45 degrees. If the patient is supine, a total lack of visible JVD is actually pathological and indicative of low volume; in this position the jugular veins are usually well-filled. (Think: flat veins in a flat patient is bad.) JVD when the head is elevated is more to our interest.

Some examples of visible JVD follow, plus some examination tips. It is recommended that you start checking this on your healthy patients now, so you’ll know what it looks like before you try to make a diagnostic call using its presence. And until you do, stop documenting “no JVD” on your assessments!

Significant JVD

Significant JVD

A different, much larger view of the same (click to enlarge)

A different, much larger view of the same (click to enlarge)

Click through for a good discussion of JVD assessment

Click through for a good discussion of JVD assessment

Some more subtle JVD

Some more subtle JVD

The basic method of measuring JVD

The basic method of measuring JVD

A nicely thick and squiggly external jugular

A nicely thick and squiggly external jugular

Here’s a student making her external jugular “pop” by heavily bearing down, aka the Valsalva maneuver. This markedly increases thoracic pressure, increasing venous backup; it’s an exaggeration of the effect seen during normal exhalation.

Another example of someone inducing JVD by a Valsalva

Here’s a great video demonstrating the appearance of JVD, how to measure it, and testing the abdominojugular reflex (formerly known as the hepatojugular), which involves pressing down on the abdomen to raise thoracic pressure.

A brief clip of jugular venous pulsation, visible mainly toward the suprasternal notch.

http://www.youtube.com/watch?v=sOpn6_r7Wo4

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Drug Families: ACE Inhibitors and ARBs

July 2, 2011 by 2 Comments

Understanding the renin-angiotensin-aldosterone system is like following one of those dotted-line Family Circus cartoons — not just long and tortuous, but seemingly designed just to be obnoxious.

Here’s the basic idea. The RAAS is the basic system your body uses to control blood pressure, as well as related values like fluid volume and sodium levels. The most important thing to understand is that the activation of this system causes an increase in blood pressure. Following the trail:

First, renin is released by the kidneys. Renin attacks circulating angiotensinogen, turning it into angiotensin I. Angiotensin I is attacked by circulating angiotensin converting enzyme (or ACE), which turns it into angiotensin II. Angiotensin II has various effects, one of which is to stimulate the release of aldosterone.

Whew.

But this isn’t as complicated as it looks. Renin has no real effect. Angiotensinogen just makes angiotensin I. Angiotensin I’s main role is to make angiotensin II. The real money here is in angiotensin II, as well as aldosterone.

Angiotensin II has the primary effect of vasoconstriction. It tightens up the vasculature, increasing blood pressure and systemic resistance. It also produces vasopressin (aka ADH, or anti-diuretic hormone) and aldosterone, which cause the kidneys to downregulate urine production — more fluid will be returned to the circulation rather than discarded into the bladder. Vasopressin also helps angiotensin II to induce further vasoconstriction.

To make a long story short, the activation of the RAAS system causes an increase in blood pressure via both vasoconstriction and a decrease in kidney output. It is always active, playing a key role in maintaining homeostasis; if you sweat out a liter of water running a marathon, or bleed out a liter from a gunshot wound, the system simply upregulates itself to maintain your blood pressure using the remaining volume. (Unlike the sympathetic and parasympathetic systems, which also play a major role in regulating blood pressure, regulation via the RAAS is captained mainly at the kidneys, where low pressure and throughput induces increased renin production.)

Cool? Cool.

Okay, so the role of ACE, or angiotensin-converting enzyme, was to transform the useless angiotensin I into the powerful angiotensin II. What do you think a drug called an ACE inhibitor would do? Indeed: it inhibits the activity of ACE, thus reducing the production of angiotensin II, which then causes reduced production of aldosterone and vasopressin.

Less angiotensin II means less vasoconstriction; the systemic circulation opens up, reducing blood pressure. Less aldosterone means less fluid is retained at the kidneys, so urine output is increased, reducing circulating volume, and again, reducing blood pressure. Handy!

A secondary role of ACE is to degrade, or break down, bradykinin. Bradykinin is basically just another vasodilator. If ACE is inhibited, then less bradykinin will be broken down, hence more bradykinin will be available. The result is more vasodilation — once again, reducing blood pressure.

Readers who can recognize patterns will probably have deduced that ACE inhibitors are used primarily to reduce blood pressure. Obviously, this includes the typical patient with primary hypertension that needs to be managed to reduce long-term morbidity. But it also means other things:

  • Reduced afterload — the resistance the heart has to push against when it pumps blood — means less work for the heart. This is beneficial for patients with heart failure, whose hearts aren’t pumping very well to begin with; or with coronary artery disease, whose hearts need to manage their workload to match the oxygen they’re able to bring in. It reduces “remodelling,” where the heart and the arteries thicken and change shape to better pump hypertensive volumes, with harmful results. And it reduces the damage following myocardial infarction.
  • Reduced preload — the amount of blood that passively fills the heart during diastole — — also means less work for the heart. Greater preload causes greater filling and hence greater contraction, which all means more work, more oxygen demand, and more remodelling. In heart failure, where the heart is unable to fully expel its contents, reduced preload also means less “extra” fluid to back up into the lungs and circulation, and therefore less edema.
  • Better renal function. This is a desirable effect in patients with various forms of kidney disease.

Angiotensin receptor blockers (ARBs) are a closely related family of drugs. Instead of interfering with the conversion of angiotensin I to angiotensin II, they simply prevent angiotensin II from binding with its receptors. The effects are therefore largely the same: vasodilation; reduced aldosterone production, with corresponding greater urine output; and reduction in hypertension with less work for the heart.

The main difference between ACE inhibitors and ARBs goes back to bradykinin. If you remember, ACE plays two roles: converting angiotensin I to angiotensin II, and degrading bradykinin, a vasodilator. Since ARBs have no effect on ACE, bradykinin is broken down normally. This may result in slightly less vasodilation, but it also reduces the side effects of elevated bradykinin, which can include edema and a nasty cough. ARBs are most often used in patients who can’t tolerate ACE inhibitors.

Overdose on ACE inhibitors is generally unremarkable. The main effect is hypotension, but it is rarely severe.

 

Examples

Generic names of ACE inhibitors and ARBs are very, very easy. Trade names are harder, but do have some common elements.

ACE inhibitors

  • Drugs ending in -pril are invariably ACE inhibitors (enalapril, ramipril, captopril, lisinopril, etc.)
  • Drugs ending in -ace are often trade names of ACE inhibitors (Altace, Tritace)
  • Drugs ending in -tec are often trade names of ACE inhibitors (Vasotec, Renitec, Novatec)

ARBs

  • Drugs ending in -sartan are invariably ARBs (losartan, valsartan, candesartan, etc.)

More Drug Families: Stimulants and Depressants; Steroids and Antibiotics; Anticoagulants and Antiplatelets

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Get Up, Stand Up: Orthostatics

May 8, 2011 by 1 Comment

Orthostatic vital signs. Nurses think they’re a pain in the neck. Some doctors think they’re of marginal usefulness. Many providers simply think they’re a dying breed.

Like many old-school physical exam techniques, though, they’re dying only because high-tech imaging and laboratory techniques have largely replaced their role. And I don’t know about you, but my ambulance doesn’t come equipped for an ultrasound or serum electrolytes. Diagnostically, EMS lives in the Olden Days — the days of the hands-on physical, the stethoscope, the palpation and percussion, the careful and detailed history. For us, orthostatics have been and still are a valuable tool in patient assessment.

How are they performed? Orthostatic vital signs are essentially multiple sets of vitals taken from the patient in different positions. (They’re also sometimes known as the tilt test or tilt table, which is indeed another way to perform them — if you have a big, pivoting table available. Postural vitals is yet another name.) They usually include blood pressure and pulse, and are taken in two to three positions — supine (flat on the back) and standing are the most common, but a sitting position is sometimes also included, or used instead of standing. This is useful when a patient is unable to safely stand, although it’s not quite as diagnostically sensitive.

Why would we do such a dance? The main badness that orthostatics reveal is hypovolemia. With a full tank of blood, what ordinarily happens when I stand up? Gravity draws some of my blood into the lower portion of my body (mostly these big ol’ legs). This reduces perfusion to the important organs upstairs, especially my brain, so my body instantly compensates by increasing my heartrate a bit and tightening up my vasculature. No problem. However, what if my circulating volume is low — whether due to bleeding, dehydration, or even a “relative” hypovolemia (in distributive shocks such as sepsis or anaphylaxis)? In that case, when my smaller volume of blood is pulled away by gravity, my body will have a harder time compensating. If it’s not fully able to, then my blood pressure will drop systemically.

“But,” you cry, “surely this is all just extra steps. Can’t I recognize hypovolemia from basic vital signs — no matter what position you’re in?”

Well, yes and no. If it’s severe enough, then it will be readily apparent even if I’m standing on my head. But we routinely take baseline vitals on patients who are at least somewhat horizontal, and this is the ideal position to allow the body to compensate for low volume. By “challenging” the system with the use of gravity, we reveal the compensated hypovolemias… rather than only seeing the severely decompensated shock patients, who we can easily diagnose from thirty paces anyway. Like a cardiac stress test, we see more by pushing the body until it starts to fail; that’s how you discover the cracks beneath the surface.

Do we run on patients with hypovolemia? Oh, yes. External bleeding is a gimme, but how about GI bleeds? Decreased oral fluid intake? Increased urination due to diuretics? How about the day after a frat party kegger? Any of this sound familiar? It would be foolish to take the time to do this when it won’t affect patient care — such as in the obviously shocked patient — but there are times when what it reveals can be important, such as in patients who initially appear well and are considering refusing transport.

Here’s the process I’d recommend for taking orthostatics:

  1. Start with your initial, baseline set of vitals. Whatever position your patient is found in, that’s fine. Deal with your initial assessment in the usual fashion.
  2. Once you’re starting to go down a diagnostic pathway that prominently includes hypovolemic conditions in the differential, start thinking about orthostatics. If your initial vitals were taken while seated, try lying the patient flat and taking another pulse and BP. If possible, wait a minute or so between posture change and obtaining vitals; this will allow their system to “settle out” and avoid capturing aberrant numbers while they reestablish equilibrium.
  3. Ask yourself: can the patient safely stand? Even in altered or poorly-ambulatory individuals, the answer might be “yes” with your assistance, up to and including a burly firefighter supporting them from behind with a bearhug. (Caution here is advised even in basically well patients, because significant orthostatic hypotension may result in a sudden loss of consciousness upon standing. You don’t want your “positive” finding to come from a downed patient with a fresh hip fracture.) If safe to do so, stand the patient and take another pulse and BP. Again, waiting at least a minute is ideal, but if that’s not possible, don’t fret too much.
  4. For totally non-ambulatory patients, substitute sitting upright for standing. Ideally, this should be in a chair (or off the side of the stretcher) where their legs can hang, rather than a Fowler’s position with legs straight ahead.
  5. For utterly immobile patients who can’t even sit upright, or if attempting orthostatics in the truck while already transporting, you’ll need to do your best to position them with the stretcher back itself. Fully supine will be your low position, full upright Fowler’s will be your high position, and a semi-Fowler’s middle ground can be included if desired.

On interpretation: healthy, euvolemic patients can exhibit small orthostatic changes, so hypovolemia is only appreciable from a significant drop in BP or increase in heart rate. From supine to standing, a drop in the systolic blood pressure of over 20 is usually considered abnormal, as is an increase in pulse of over 30. (Changes from supine to sitting, or sitting to standing, will obviously be smaller, and therefore harder to distinguish from ordinary physiological fluctuations.) A drop in diastolic pressure of over 10 is also considered aberrant. You can remember this as the “10–20–30” rule.

Try to remember what’s going on here. As the patient shifts upright, their available volume is decreasing, for which their body attempts to compensate — in part by increasing their heart rate. It’s a truism that younger, healthier, less medicated patients are more able to compensate than older and less well individuals. So for the same volume status, you would be more likely to see an increase in pulse from the younger patient, perhaps with no change in pressure; whereas the older patient might have less pulse differential but a greater drop in pressure. (On the whole, the pulse change tends to be a more sensitive indicator than pressure, since almost everyone is able to compensate somewhat for orthostatic effects. As always, if you look for the compensation rather than the decompensation — the patch, rather than the hole it’s covering — you’ll see more red flags and find them sooner.)

Are substantial orthostatic changes definitive proof of hypovolemia? No, nothing’s certain in this world. Another possible cause is autonomic dysregulation, which essentially means that the normal compensating mechanisms (namely baroreceptors that detect the drop in pressure and stimulate vasoconstriction, chronotropy, and inotropy) fail to function properly. You do have enough juice, but your body isn’t doing its job of keeping it evenly circulating. Vasovagal syncope is one common example of this; I’ve got it myself, in fact, and hence have a habit of passing out while squatting. This sort of thing is not related to volume status, although if you combine the two the effect can be synergistic. A good history can help distinguish them: ask the patient if they have a prior history of dizziness upon standing.

Finally, pulse and pressure are not the only changes you can assess. One of the best indicators of orthostatic hypotension is simply a subjective feeling of light-headedness reported by the patient. Although sudden light-headedness upon standing can have other causes (the other big possibility is benign paroxysmal positional vertigo — although strictly speaking, BPPV tends to cause “dizziness,” which is not the same as “lightheadedness”), hypovolemia is certainly one of the most likely. So stand ’em up when it’s safe and reasonable, ask how they feel, grab the vitals if you can, and maybe even take the opportunity to see how well they walk (a nice, broad neurological test — the total inability to ambulate in a normally ambulatory patient is a very ominous sign).

Orthostatics are usually recorded on documentation by drawing little stick figures of the appropriate postures. For those who find this goofy, or are documenting on computers without “stick figure” keys, a full written description will do.

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The Rhythm Method

April 24, 2011 by 1 Comment


One two three — five six seven

What’s the missing number?

If you said four, congratulations. You have a basic human ability to recognize patterns — one of the best tools we have to separate us from the monkeys and sea-slugs.

One of the simplest types of pattern is a rhythm, and the simplest rhythm is a steady cadence. Ba-dump, ba-dump, ba-dump. Imagine a metronome or a drummer tapping out a fixed, continuous pace at an unchanging rhythm.

This is also one of the most basic and useful tricks you’ll ever use when taking vitals!

See, measuring vitals involves feeling, hearing, or observing a series of fairly subtle blips over a period of time. Unfortunately, interference is common in the field, and it’s a rare day when bumps in the road and bangs in the cabin don’t eat up at least one of those blips.

When taking a radial pulse, if over 15 seconds you count 18 beats, you have a pulse of 72; but if just a couple of those beats are lost due to your movement or the patient’s, suddenly it becomes 64, which is a substantial difference. This is no good; we want better reliability than that.

Rhythm is the answer. A pulse is typically a regular rhythm. So are respirations. So are the Korotkoff sounds of a blood pressure. In order to establish this rhythm, you only need to hear two consecutive beats, and appreciate exactly how far apart they are. If you can do this, then you can continue to mentally tap out that pace — hopefully, while continuing to feel, see, or hear the true beats, which will help you to maintain the right speed, but even if you miss some, you’ll still have your mental beat to count. Even if you miss most of them!

So you feel for the pulse, and you palpate the first couple beats. Then you hit a tortuous section of road that throws you around the cabin, and you’re unable to feel anything for several seconds. But you already had the rhythm in your head, so when you pick up the pulse again, you haven’t lost the count — and you’ll end up with an accurate number.

Now, in sick people these rhythms aren’t always regular. And if you observe that a pulse or respiratory cycle isn’t regular, then this system won’t be as effective — for instance, there’s not much point in trying to find the “beat” to an A-Fib pulse. But small irregularities or breaks in the rhythm are okay, as long as there’s still a regular cycle underlying it; for instance, occasional dropped (or extra) beats won’t change the basic rate.

Give it a try. If you got rhythm, vital signs will never give you trouble again.

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Vital Signs: Blood Pressure

March 20, 2011 by 4 Comments

For other Vital Signs posts, see: Respirations and Pulse

In the grand scheme of medical skills, taking a manual blood pressure is far from difficult, but sick people and austere conditions can combine to make it another thing entirely. Obtaining a BP on an ill patient while rattling down the road is legitimately one of the most difficult psychomotor skills an EMT-Basic has to master.

Mastering it starts with stacking the odds in your favor. A good stethoscope is better than a lousy one — you don’t need a $500 cardiology model, but something with good insulation and tight-fitting earpieces can make a real difference. Of course, you’ll also want to try to take your blood pressures at times of peace: on scene, before the rig starts moving, or even shoehorned in while stopped at traffic lights.

The elbow-supported technique for finding the brachial pulse is also ideal for taking a BP; trying to hear anything when the arm is slightly flexed is a recipe for frustration. But ensure that however you arrange things, the arm is completely relaxed, because muscular tension can radically throw a measurement; this will require fully supporting the arm and sometimes reassuring the patient. “Just relax” is the line I always deliver while busily pumping the bulb.

Where to put the gauge? Wherever. I’ll usually clip it to one of the stretcher straps, but you can find a bit of blanket that it’ll nestle into, secure it to a shirt, clip it to your watchband or the edge of the cuff, or just ask the patient to hold it for you. The built-in strap on the cuff is only a good location if you’re at the patient’s right side, which is typically not where we sit while we’re transporting. There’s probably a huge market niche out there for “EMS style” cuffs with their handedness reversed… but I digress.

Although I don’t always follow all of these steps, here’s the basic approach I recommend for a routine blood pressure check:

  • Support the arm, ideally at a position that is horizontally level with the heart.
  • Palpate the antecubital fossa until you find the pulse point. Note this location.
  • Palpating at the radial or the AC, pump up the cuff until you lose the pulse. Note this number and deflate the cuff.
  • Place your scope on the AC and inflate the cuff past the previous number. Obtain your pressure in the ordinary fashion.

Starting with a palpated pressure may seem redundant, and it can be, but it has two advantages: first, it gives you a rough sense of what systolic to look for, and second, if you’re unable to auscultate a pressure, you’ll still have a palpated one to record. This is actually the officially recommended method, although it seems rarely done nowadays.

Palpated pressures are legitimate, although when they start becoming the norm it can be a sign of lazy care. The diastolic can be a valuable number, though, particularly in traumatic or cardiac cases, so remember that auscultating is still the default standard of care. And remember, particularly if you’re mixing methods, that palpated pressures often will differ from auscultated pressures (including those taken by machine), usually by 10-15 points on the low side.

What if you’re not getting anything from the arm? Well, you can try the other arm, of course. But really, the thing to remember is that you can take a blood pressure anywhere there’s a pulse, although it’s much easier when that pulse is strong and the artery proximal to it can be easily occluded. Remember that although you can palpate a pressure from any distal spot on the same artery, near or far (barring anastamoses), auscultation — which is essentially listening to the turbulence created immediately downstream of the occlusion — requires placing your scope just below the cuff, and will not be successful farther downstream. Putting the cuff (pedi cuffs when needed) on the forearm and measuring at the radial is effective; thigh cuffs work too, although the popliteal can be an evasive pulse to locate. You can even cuff the lower calf and palpate a pedal or tibial pulse, if you’re daring. Go nuts, and try to experiment before the call when you actually need it. Do make an effort, though, to use an appropriate sized cuff for the extremity; mis-sized cuffs can actually yield significantly erroneous readings. For the morbidly obese, I usually prefer to place a regular cuff on the forearm than to use a thigh cuff on the upper arm, but see what works for you.

As a final note, remember that cuffing the neck and palpating the temporal pulse is never an appropriate method of patient assessment, no matter how little blood you may suspect is reaching their brain.

On maintenance: during your morning checkout, pump some air into the cuff, close the valve and give the whole thing a squeeze to check for leaks. There’s nothing better than discovering these after you’ve wrapped it around a critical patient’s arm.

On sphygmomanometers: for obvious reasons, the resting point for the needle should be at zero. (Very cheap cuffs sometimes have a pin-stop here for the needle to rest against; this is a problem because the dial can be miscalibrated without showing it. Pin-stop gauges shouldn’t be used unless your service is seriously broke.) If you have one that needs zeroing, most cuffs can be adjusted by pulling the tubing off the dial, grasping the metal nipple with some pliers (or very strong fingers), and twisting it in either direction until the needle is zeroed. Alternately, fans of mental math can just add or subtract the false “zero” number each time they take a pressure.

And finally, on tourniquets: the immortal Dr. Scott Weingart of Emcrit has described his practice of using BP cuffs as tourniquets. You’ll hear about this from time to time, but there’s always someone who points out the damned things leak like sieves and that’s the last property you want in a tourniquet. Dr. Weingart’s solution is to pump up the cuff until bleeding is controlled (or 250mmHg, whichever is sooner), then clamp both tubes with locking hemostats. (He uses smooth ones to avoid damaging the rubber; he recommends padding with a 4×4 if you’re using a ridged hemostat.) My hemostats are all in the shop, and this may or may not fly with your agency — modifying equipment for “off-label” use is always somewhat shaky ground for us field peons — but I think it’s a splendid idea if you can swing it.

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