Without evidence of benefit, an intervention should not be presumed to be beneficial or safe.

- Rogue Medic

Blood volume prior to and following treatment of acute cardiogenic pulmonary edema


One of the myths of treatment for CHF/ADHF (Congestive Heart Failure/Acute Decompensated Heart Failure) is that the patients are fluid overloaded. We MUST make the patient pee.


If you want to live, you have to pee!


Image credit.

Pee or die!


This has been studied. all the way back in 1978 –


The normal patients had 22% more total plasma volume.

The normal patients had 21% more total blood volume.

The need to remove fluids is based on what?

It is interesting that this study was of patients treated with oxygen, morphine, and furosemide. Only oxygen is still important in the acute treatment of CHF/ADHF.

There were no significant differences in the parameters measured or calculated between nine patients with prior history of acute pulmonary edema and the 12 patients in whom pulmonary edema occurred for the first time. There were also no significant differences in these parameters between the 11 patients who had been previously treated with diuretics and the remaining ten patients.[1]


We give have been trained to give furosemide (Lasix – frusemide in Commonwealth countries) because CHF = Too much fluid.

How long do we need to hold on to our myths?

How long can we perpetuate dangerous traditions?

Afterward, these patients need to receive fluid, because we have made them even more dehydrated – for no benefit.

Correction – These appear to be ICU (Intensive Care Unit) patients. I had mistakenly assumed these were ED (Emergency Department) patients. This also weakens the conclusions I was drawing from the study. I had been misreading the Center for the Critically Ill as a fancy name for the ED (A&E in Commonwealth countries).

Read Doesn’t that study prove Lasix works? for a more in depth explanation.


[1] Blood volume prior to and following treatment of acute cardiogenic pulmonary edema.
Figueras J, Weil MH.
Circulation. 1978 Feb;57(2):349-55.
PMID: 618625 [PubMed – indexed for MEDLINE]

Free Full Text Download from Circulation in PDF format

Figueras J, & Weil MH (1978). Blood volume prior to and following treatment of acute cardiogenic pulmonary edema. Circulation, 57 (2), 349-55 PMID: 618625

Edited 12-27-2018 to add the necessary paragraph explaining that this is not an ED study and the link to where I provide more detail.


The Benefits of Lasix in CHF

Furosemide (Lasix) does not improve outcomes for the very sick CHF (Congestive Heart Failure or ADHF – Acute Decompensated Heart Failure) patients.

There are basically three mechanisms for CHF –

  • PRE-load
  • Contractility
  • AFTER-load

The problem is not the PEE-load, unless there is some anatomic connection between the kidneys and the lungs that I do not know about

But what about the circulatory system? The circulatory system connects the lungs and the kidneys and allows the kidneys to remove fluid from the circulation, which allows the fluid to wander out of the lungs.


Stable patients seem to tolerate Lasix well, but these patients will tolerate almost anything we do to them.

Unstable patients are a little harder to keep alive.

What happens to the circulation to the kidneys under stress – the kind of stress that one might experience when not able to get enough oxygen?

The kidneys shut down.

Closed for business.

Take your Lasix somewhere else.

Comeback after the patient’s kidney circulation is open for Lasix again.

Image source.

It is better to NOT understand something true, than to understand something false – Example 1

Continuing with my explanation of the problems with wanting explanations for why something happens. Why something works. Why something doesn’t work.

The why is not the important part. What we need to know are –

What we can expect to happen.

Under what circumstances we can expect it to happen,

At what rate we can expect it to happen.

What complications we should watch for.


It is better to not understand something true, than to understand something false. – Neils Bohr.


For example, some people explain the effects of furosemide (Lasix) on acute CHF (Congestive Heart Failure) with some variation of the following –


Furosemide makes acute CHF better by moving fluid from the lungs to the bladder.


This is false.


If we believe (understand) the above false statement, that is dangerous for patients. We are likely to treat patients with furosemide, which has a nice story, but the story is false.

Even if we do not understand why CPAP (Continuous Positive Airway Pressure) and High-Dose NTG (NiTroGlycerin) are excellent treatments for acute CHF, we can still give them to patients and improve patient outcomes.

The side effects of furosemide may cause more harm than any benefit furosemide might provide in the emergency setting. Most of these patients are dehydrated and need to be given fluid in the ED (Emergency Department). Furosemide temporarily raises the blood pressure, but it is almost always more important to lower the blood pressure. Furosemide is for fluid overloaded patients, but acute CHF patients are usually not fluid overloaded – the fluid is just in the wrong place.

Furosemide does not transfer fluid from the lungs to the bladder.


It is not important to know why this magic does not happen. We only need to know that it does not happen.

Does removing excess fluid from the body help stable CHF?

If the CHF is due to fluid overload, then furosemide probably does help stable patients. We are not really interested in what works when the patient is stable. We are interested in what works when that patient is no longer stable – the emergency patient.

If we dehydrate the body even more, then that may pull some fluid out of the lungs, but that is not making things better.

The patient is hypertensive and dehydrated with wet lungs.

We want to fix all 3 of the problems. Our goal is not to make one of the problems worse and hope that miraculously fixes the other 2 problems.

See also EMS NTG for CHF – Bolus or Infusion – Part II.

Added 02/05/2012 @ 14:00 – An example pertinent to today – Super Bull Sunday on the manufactured explanation for a non-existent rise in domestic violence on the day of the Super Bowl from snopes.com.


Do Drug Shortages Really Impact EMS? – Answer 3

Here is part 3 of the details from the points I raised in commenting on the discussion of the drug shortages and the way these affect EMS. Do Drug Shortages Really Impact EMS? – EMS Office Hours and followed by Do Drug Shortages Really Impact EMS? – Answer 1, then by Do Drug Shortages Really Impact EMS? – Answer 2. This is broken up by answer. There are many points covered for a podcast that lasts less than 40 minutes. Do Drug Shortages Really Impact EMS?

3. Should we switch from Lasix to Bumex?

This presumes that filling the patient’s bladder is the best, or second best, or third best, or even just not the worst way for EMS to treat patients with heart failure.

Filling the bladder with fluid does not mean that we removed the fluid from the lungs.

Where is it taught that the lungs drain into the bladder?

Where is the evidence that any diuretics are in any way beneficial for the pre-hospital treatment of the patient who does not have peripheral edema?

Where is any evidence that any diuretics should ever be used before any of the other treatments (CPAP, NTG, High-dose NTG, ACE inhibitors, et cetera) for the pre-hospital treatment of heart failure?

Why should EMS be giving so many different treatments to a single patient?

The more treatments we give, the more likely that we the patient will have complications.

The more treatments we give, the less likely that we can figure out what caused the complications.

Where is there any evidence that these complications are good for patients?

One person on the show mentions the problems with kidney injury from Lasix. That is just one of the reasons for not using diuretics. Another problem is that medics too often give diuretics for pneumonia. This is a training and oversight issue, but that is just another example of where medical directors are failing patients.

If paramedics are treating pneumonia with diuretics, why aren’t the medical directors aware of it?

If medical directors do know that paramedics are treating pneumonia with diuretics, why aren’t the medical directors doing something about it?

How can paramedic schools graduate people who can’t tell the difference between pneumonia and heart failure?

How can paramedic schools graduate people who treat pneumonia with Lasix or Bumex?

While there can be problems differentiating between pneumonia and heart failure, if I am not able to clearly identify the condition as heart failure, I should never give Lasix or Bumex.

If I hear crackles, presume heart failure, and give Lasix, because Lasix can’t hurt, then I probably should not be a paramedic.

If I allow a medic to treat something that sounds like crackles as heart failure, because Lasix can’t hurt, then I probably should not be a medical director.

We need better paramedics.

We need to ridicule the bad paramedics that we do have.

We need better medical directors.

We need to ridicule the bad medical directors that we do have.

Continued in –
Do Drug Shortages Really Impact EMS? – Answer 4


Furosemide and Drug Shortages 2

Also posted over at Paramedicine 101, which is now at EMS Blogs. Go check out the excellent material there.

I will keep pointing out the problems with furosemide (Lasix) and the evidence against it. Let’s ignore the problems with giving furosemide to patients who actually have CHF/ADHF (Congestive Heart Failure/Acute Decompensated Heart Failure). Can medics correctly identify CHF/ADHF?

The EHS ePCR database identified paramedic reports in which furosemide was administered. As furosemide only appears in the CHF/pulmonary edema protocol, paramedic differential diagnosis of this was assumed by furosemide administration. Data abstraction from the EHS ePCR and ED chart included the EP primary diagnosis, considered the gold standard. Other data points collected included: demographic information; EHS treatment administered; treatment administered in the ED; adverse events and patient disposition.[1]

They do not describe their method of selecting the charts.

Was it completely random?

Was it sequential?

How did they select their sample?

There were three objectives of this study. The first was to determine agreement between paramedic administration of furosemide with EP diagnosis of CHF. The second was to examine differences in interventions administered by paramedics and in the ED by EP diagnosis of CHF. The third objective was to identify any adverse events that occurred during patient care.[1]

How much agreement on CHF/ADHF diagnoses?

It should be noted that seven patients without an ED diagnosis of CHF received ED furosemide and 43 patients received ED nitro with only eight of those having a primary diagnosis of ACS. This data put the accuracy of the primary ED final diagnosis as a reference standard into question, as it appears CHF may have been in the differential diagnosis for many patients not ultimately diagnosed with CHF. Secondary diagnoses were not sought out and included. Therefore, paramedic accuracy reported in this study may be falsely low, if CHF was part of the EP secondary diagnoses. It should also be noted that there were two patients with a diagnosis of “shortness of breath not yet diagnosed.” It is possible that these patients did indeed have CHF, but were not diagnosed until a later time during hospital care. This needs to be considered when determining paramedic diagnostic accuracy.[1]

OK. For some reason, the emergency physicians gave furosemide to 21% of the patients they diagnosed with something other than CHF/ADHF. That may be explained by the CHF/ADHF being a secondary diagnosis.

This is something that should have been included in the study. What was being treated and for what reason. From the way they describe their data, they had the actual ED physician chart, not just a diagnosis. This is something they should include in a follow-up study, especially with a larger sample size.

Since two of the patients had the diagnosis shortness of breath not yet diagnosed I will move them to the CHF/ADHF side of the graph. After all, most of the patients were diagnosed with CHF/ADHF.

That looks so much better.

On the other hand, there are problems with the way they conclude that some patients do not have CHF/ADHF. How much higher would things be if secondary diagnoses were included?

It should be noted that seven patients without an ED diagnosis of CHF received ED furosemide and 43 patients received ED nitro with only eight of those having a primary diagnosis of ACS. This data put the accuracy of the primary ED final diagnosis as a reference standard into question[1]

What does NTG (NiTroGlycerin) have to do with ACS (Acute Coronary Syndrome), when examining CHF/ADHF treatment?

NTG is the most effective medication for hypertensive CHF/ADHF. Go listen to the EMCrit CHF/ADHF podcast if you doubt me. For those not hypertensive, this research certainly suggests that NTG should be studied.

NTG is not just for chest pain.

Data abstraction from the EHS ePCR and ED chart included the EP primary diagnosis, considered the gold standard.[1]

Maybe. Maybe not. And don’t get me started on Gold Standards.

ED mortality was higher in patients with an alternate diagnosis than those diagnosed with CHF by the EP (2/60 vs. 6/34, p=0.017). As documented on ED charts, eight patients in this sample suffered adverse events other than death. These adverse events were: hypotension (n =3), heart rate problem (n =3), electrolyte imbalance (n =1), and respiratory effort decline (n = 1). All of the patients who suffered adverse events were diagnosed with CHF by the EP. Adverse events were not associated with the amount of nitroglycerin, morphine or furosemide administered.[1]

Adverse events in the ED were documented as occurring as often as death in the ED. Almost all of the deaths were in the group not diagnosed with CHF/ADHF, but all of the adverse events occurred in the group diagnosed with CHF/ADHF.

Of the six patients with an alternate diagnosis who had an outcome of death, three were diagnosed with pneumonia. Eight adverse events other than death were identified in this sample. Interestingly, all these patients were correctly identified as having CHF, which contradicts previous research which has found adverse events were more likely in patients incorrectly treated for CHF by paramedics.11,12 This indicates that furosemide should be administered with caution, even in cases where diagnosis of CHF is correct.[1]

Where is the evidence that furosemide should be administered, even if the diagnosis of CHF/ADHF is correct?

What would we want to know?

Did the patients have peripheral edema when given furosemide by EMS. Even with peripheral edema, furosemide is far from the first line drug, but without peripheral edema, it is not going to do anything good.

These patients need the best treatment possible, not the most persistent hold out from the Dark Ages.

We have known that CHF/ADHF is not primarily a fluid overload problem since the 1980s.

Why is EMS still using furosemide?

Is there any problem with a shortage of furosemide?

Not at all, but this isn’t the study to prove it.

I hope the authors use what they learned from this to design a definitive study of the prehospital use of furosemide.

Updated 02-07-11 to correct the uselessness of the original charts I made for this post.

More details are in Corrections of Misleading Charts.


[1] Correlation of paramedic administration of furosemide with emergency physician diagnosis of congestive heart failure
Thomas Dobson, Jan Jensen, Saleema Karim, and Andrew Travers.
Journal of Emergency Primary Health Care
Vol.7, Issue 3, 2009
Free Full Text . . . . . . . Free Full Text PDF


More on Lasix in EMS

Some people may think that I am crazy for claiming that we should not use Lasix (furosemide). For a slightly different perspective, here is an emergency physician describing the appropriate treatment of unstable hypertensive acute pulmonary edema patients.

EMCrit is an excellent podcast blog with nice short podcasts. More important than being nice and short, the podcasts are science-based and address many of the issues that EMS treats. The first podcast from EMCrit is 10:33.

How important is furosemide?

Is the furosemide drug shortage important?

So, the first thing you do is get your Lasix . . .



















So, the first thing you do is get your Lasix and you throw it in the trash.


I was right.

This is the podcast for me.

It’s not going to help you and it’s very potentially going to hurt you. No Lasix in these patients. Now, I’m sure your EMS providers have already given it. Well, that’s just fine, but you don’t have to exacerbate the problem. Most of these patients will end up volume depleted, not volume overloaded when you look at their intravascular space. You’re probably going to end up giving fluid to these patients, not trying to diurese them. The problem is not fluid overload.

Most of these patients will end up volume depleted,

Go listen.

10 minutes 33 seconds of somebody who understands CHF(Congestive Heart Failure)/ADHF (Acute Decompensated Heart Failure). And he isn’t subtle. 🙂

PS – Dr. Weingart, why not try to get those of us in EMS to improve our care of these patients, too?

High-dose NTG and CPAP are also treatments that can be given by EMS. In some places, these are given by EMS.

With sublingual NTG (NiTroGlycerin) we probably cannot give too much to these patients.

We should be using NTG by IV in EMS. In Pennsylvania, IV NTG is an optional drug for 911 services.

EMCrit’s page of references supporting this aggressive approach.

Updated 02/08/11 to reflect the new blog address for EMCrit. http://emcrit.org/ The old links did not redirect appropriately.


Drug Shortages Affect Those Still in the Dark Ages – Furosemide


Also posted over at Paramedicine 101 and at Research Blogging.

Go check out the excellent material at both sites.

In the current JEMS, there is an embarrassing article. Drug Shortage Possible in N.Y.

It seems that the drugs that people are worried about are lidocaine, furosemide, 50% dextrose, and epinephrine 1:10,000 preloaded syringes. Here, I will discuss furosemide.

Furosemide is not appropriate for EMS patients, because there are more appropriate drugs, more appropriate other treatments, and it is too often given to patients who have pneumonia.

Fluid accumulation in the lungs associated with APE, until recently, was attributed to excess accumulation of total body fluid. Accordingly, treatment of APE was aimed at removing excess fluid from the lungs by promoting massive diuresis. However, this explanation for APE could not reconcile the fact that APE typically occurs during early morning hours when fluid intake is minimal. The current explanation is that APE results from fluid redistribution within the body whereby a part of the intravascular volume is redistributed to the lungs as a consequence of increased intravascular pressure as outlined above.13 Primary objectives for the treatment of acute CHF are to reduce pulmonary capillary pressure, to redistribute pulmonary fluid, and to improve forward flow.12,13 These may be achieved by reducing LV preload and afterload, providing ventilatory and inotropic supports, and identifying and treating the underlying etiology of the syndrome (Table 3). It should be recognized that these treatment measures are intended for APE patients who are normotensive or hypertensive and not those who are hypotensive. The latter comprises cardiogenic shock secondary to severe LV systolic dysfunction; treatment of these critically ill patients is beyond the scope of this review.[1]

That is a big paragraph, but there is a lot of information in there. Enough to convince us that we should not be using furosemide to treat an acute onset/exacerbation of heart failure.

In the chart below, before furosemide in treatment there are plenty of other treatments. Notice that only oxygen comes before NTG (NiTroGlycerin) and the more severe the symptoms, the more NTG is given.

Mild symptoms – One 0.4 mg NTG spray/tab – repeated every 4 to 5 minutes.

Moderate symptoms – High-dose NTG, which is explained below.

Severe symptoms – Two to five 0.4 mg sprays/tabs at a time – repeated every 3 to 5 minutes.

But, but, but, but, but, . . . . . we can only give a maximum of 3 NTG – ever.

Then you need to get a better medical director, because your medical director has you killing patients.

Am I being too subtle?

Another treatment that is very effective is CPAP (Continuous Positive Airway Pressure) which is a BLS (Basic Life Support) skill, except where medical directors like to kill patients. When using CPAP (a form of NIPPV – Non-Invasive Positive Pressure Ventilation), NTG paste can be applied. Do not be shy with the paste, because nothing is absorbed well through the skin when the skin is pale. Pale means a lack of circulation. Also, since the appropriate dose is much more than standard NTG dosing, there is not much reason to hold back.

I disagree about the placement of CPAP at the bottom. CPAP should be started right away. This was published in 2003, so it is kind of old and conservative.

You call that NTG use conservative?!?!?

I do. I have given dozens of NTG in a period of 10 to 20 minutes and never had a patient experience any adverse effects while in my care or at the hospital. I have written elsewhere about the superstitious way we approach NTG.

Furosemide is in there, but only if the patient has peripheral edema. If there is no peripheral edema, is fluid overload the problem? That is a fluid redistribution problem. There is fluid in the wrong place, but that does not mean that the whole body is overloaded with fluid or that putting a bunch of fluid in the bladder is going to make things better. Moving fluid to the bladder does not mean that we are removing it from the lungs any more than we are removing fluid from anywhere else.

Click on the chart to make it bigger. I know I can’t read any of it at this size. This is from the same paper as the paragraph above.

Well, that is just one paper. Nobody else would be so irresponsible as to recommend such large doses of NTG.

Then let’s read about what they do in the ED (Emergency Department).

Most patients who experience CPE, however, do not have ECG evidence of an acute dysrhythmia or AMI. Treatment should therefore be aimed at redistributing the excessive pulmonary interstitial fluid into the systemic circulation, which improves alveolar oxygen-carbon dioxide exchange and hypoxia; therefore, pharmacologic agents that provide preload reduction and afterload reduction should be administered. In some cases, inotropic support is required also.[2]

What drugs do we use to provide preload reduction and afterload reduction?

The most effective and rapidly-acting preload-reducing medication is nitroglycerin (NTG) [21–25]. Multiple studies have demonstrated the superiority of NTG over furosemide [21,24,26–28] and morphine sulfate [28–30] for preload reduction, symptomatic improvement, and safety. NTG can be administered in sublingual, IV, or transdermal form, although the transdermal absorption can be erratic in the patient in extremis. NTG also has the benefit of a short half-life; therefore, if the patient develops a precipitous fall in blood pressure (generally uncommon in CPE {Cardiogenic Pulmonary Edema} patients), the blood pressure should return to previous values within 5 to 10 minutes of discontinuation of administration.[2]

But what about the dose?

In one study [26], 3 mg IV boluses of NTG were administered every 5 minutes to patients who had developed CPE, a dose equivalent to a 600 mg/min infusion. This protocol was found to be safe, well-tolerated, and effective for these patients and associated with reduced need for mechanical ventilation and more rapid resolution of symptoms. Standard anti-anginal dosages of sublingual NTG with which most physicians are comfortable (ie, 400 µg every 5 minutes), has the bioequivalence of an IV NTG infusion of 60 to 80 µg/min. Physicians should, therefore, be comfortable with the safety of even higher dosages of NTG for patients who experience CPE and usually present in a hyper-adrenergic state with moderately-to-severely elevated blood pressures.[2]

That is 7 1/2 times to 10 times the standard dose of NTG – with no problems.

Maybe that maximum of 3 NTG is something that should be ignored. The AHA (American Heart Association) seems to be ignoring it. Just try to find a limit on NTG administration in the current ACLS, which is from 2005.

These papers are available in PDF format, so you can print them out and hand them to your medical director and/or to the other doctors in the ED.

These are important papers. Both are review articles. One is written for EMS, while the other is written for the ED.

If you are feeling aggressive, maybe you can write on the bottom, Call me about improving the protocols we use to treat our patients.

There is one problem with this. This will lead to fewer intubations.

The best intubation is the intubation that is prevented by excellent patient care.


[1] Prehospital therapy for acute congestive heart failure: state of the art.
Mosesso VN Jr, Dunford J, Blackwell T, Griswell JK.
Prehosp Emerg Care. 2003 Jan-Mar;7(1):13-23. Review.
PMID: 12540139 [PubMed – indexed for MEDLINE]

Free Full Text PDF

[2] Modern management of cardiogenic pulmonary edema.
Mattu A, Martinez JP, Kelly BS.
Emerg Med Clin North Am. 2005 Nov;23(4):1105-25. Review.
PMID: 16199340 [PubMed – indexed for MEDLINE]

Free Full Text PDF

Mosesso VN Jr, Dunford J, Blackwell T, & Griswell JK (2003). Prehospital therapy for acute congestive heart failure: state of the art. Prehospital emergency care : official journal of the National Association of EMS Physicians and the National Association of State EMS Directors, 7 (1), 13-23 PMID: 12540139

Mattu A, Martinez JP, & Kelly BS (2005). Modern management of cardiogenic pulmonary edema. Emergency medicine clinics of North America, 23 (4), 1105-25 PMID: 16199340


TOTWTYTR vs. Indoctrination in Iatrogenesis

Too Old To Work, Too Young to Retire has an excellent post about, well his title gives it away.

The One where he Rants about EMS Education

TOTWTYTR is right on target with this latest post. Mandatory reading for everyone involved in EMS.

In paramedic school, which is ALS (Advanced Life Support), the approach to airway management seems to be that medics will intubate the patient, so they do not need to be good at the BLS (Basic Life Support) aspects of airway management. The result is medics who do not understand the most essential part of airway management. There is nothing more important than competence in BLS airway management. Assessment is critical to competent BLS airway management, but there are plenty of medics who do not recognize esophageal tubes. Do they understand airway? Even a little bit? No.

Where is the assessment? Playing peek-a-boo with the life of the patient. Now it’s here! Now it’s not!

There should not be ALS without excellence in BLS. Teaching ALS without confirming and reinforcing excellence in BLS is bad instruction.

The medical directors for these schools should not allow this. The instructors should not, either. Nor should the students allow this.

Of course as you move from sentence to sentence, in the previous paragraph, the order of responsibility is dramatically decreasing. We should not expect the students to take responsibility for the curriculum. A bunch of people think that the medical director, the one who says that idiocy is permitted or that idiocy is not permitted, should not be held accountable for the results of his actions.

We allow medical directors to set up a system that proclaims:

Idiocy, Incompetence, and Iatrogenesis are permitted here.


If you look at what happens when these students have graduated and are developing as medics, the next big influence on the way they treat people is, surprise, surprise, the EMS medical director.

I believe that the difference between the ALS services that have excellent quality and the rest . . . .

What do you mean the rest?

There is no bronze medal in medical care, unless you believe in the government quality indicator rankings.

There are places that uniformly provide excellent care.


After excellent it is just a matter of naming the abuses the patient may suffer.

Statistically, many of these patients will arrive at the hospital unharmed, but there will be plenty who do not escape harm. So, what method of medical misadventure will they come up with this time?

I believe that the difference between the ALS services that have excellent quality and the rest lies in the involvement of the medical director.

An absentee medical director means that on a regular basis these are some of the medical misadventure menagerie that the medics will be inflicting on patients:

  • Unrecognized esophageal tubes,
  • Furosemide (Lasix) for pneumonia,
  • Delayed transport for IVs,
  • Patients treated according to the dispatch information instead of their actual medical condition,
  • Poor pain management,
  • Et cetera.
Absentee = Not being there.

  • Performing chart review is the same thing as not being there, because you aren’t.
  • OLMC (On Line Medical Command) requirements are the same as not being there, because you aren’t.
  • Having monthly/quarterly/yearly continuing education is the same as not being there, because you aren’t.
  • Telemetry (transmitting ECGs to be read by the doctor) is the same thing as not being there, because you aren’t.
  • Et cetera.
Being there to take report from medics at the hospital, showing up on calls, following up (with the patient and with hospital staff) on all unstable patients, . . . . are part of being there.

Do you know your medics?

Investing in some smart technology is a good thing (waveform capnography) when it is part of improving the abilities of the medics. Investing in telemetry is just a waste of money, an admission that you are trying to keep it stupid, and that you don’t know how to run ALS. Spending money on technology instead of a medical director, who WILL be there, is a waste of money.

Idiocy, Incompetence, and Iatrogenesis are permitted here.

Would you want this inscription on your certificate/diploma/degree?

Would you want this inscription on the side of your ambulance?

Would you want this inscription on your EMS patch?

The NR (National Registry of EMTs) should come up with a nice round patch EMT-P-III?

This is not the New York level of EMT-III (intermediate). It is quite a bit different.

Iatrogenesis = inadvertent and preventable induction of disease or complications by the medical treatment or procedures of a physician.

Being There, the book or movie, is not the same as a medical director being there.