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

- Rogue Medic

Lasix Kills: Better Therapy for CHF

Wed, 07 Nov 2012 15:30:49 -0500 by
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EMS Expo had several excellent presentations and a lot of good company. One of my favorite topics was covered by one of my favorite doctors, Keith Wesley.[1] Attend his presentations if you have the opportunity.

For emergency treatment of CHF (Congestive Heart Failure), furosemide (Lasix – frusemide in Commonwealth countries) is a bad drug.

If we use Lasix, are we killers?

Maybe.

How much follow up do we get on our patients?

How would we know if we dehydrate a patient and alter his electrolytes to the point of killing him?

How would we know that the increase in blood pressure from Lasix is not making the CHF worse?

What if we give Lasix to someone with asthma, or pneumonia, or a PE (Pulmonary Embolus), are we shortening the lives of these patients?

How many of these patients die and how many might not die if they never received Lasix from EMS or from the ED?

We do not know, but we would have to be insane to think that the number is zero – or even close to zero.
 

Where does Lasix work?

In the kidneys, when there is good circulation to the kidneys – not in the patient who is pale, cool, and sweaty, because that is an indication of catecholamine release.

Some claim that Lasix will cause vasodilation and that this will improve outcomes.
 

Lasix causes vasoconstriction.
 

Vasoconstriction is what kills CHF patients.
 

Does Lasix kill?

Yes. Lasix kills.
 

In patients with chronic heart failure and especially in the presence of generalized edema, prior investigations have demonstrated either increases in intravascular volume17-19 or no consistent changes.20 During acute cardiogenic pulmonary edema, however, blood volume is more frequently reduced. In 16 of the 21 patients herein reported, the initial volume measured or calculated after onset of acute dyspnea demonstrated a lower than normal intravascular volume. To this extent, volume changes during acute pulmonary edema differ from those which were observed during chronic congestive heart failure.[2]

 

Chronic CHF and Acute CHF are not the same and should not be treated as if they are the same.

Lasix is safe for chronic CHF.

Lasix is not safe for acute CHF.

We need to lower the blood pressure, but Lasix raises the blood pressure.
 

Two patients became noticeably shorter of breath by 10 to 20 minutes after furosemide administration.[3]

 


 

We need to lower the heart rate, lower the blood pressure, and decrease the amount of work being done by the heart. Heart failure means that the heart is already having trouble.

The solution is not to make the heart work harder.
 

Activation of the sympathetic nervous system by intravenous furosemide treatment in patients with congestive heart failure is a new finding.[3]

 

New?

The paper was written in 1985, but we keep hearing that Lasix is a vasodilator.
 


 

Lasix raises blood pressure in emergency treatment of CHF.

Lasix raises heart rate in emergency treatment of CHF.

Lasix decreases cardiac output in emergency treatment of CHF.
 

Lasix makes acute CHF worse.
 

For the first hour, or more, the effects of Lasix are dangerous to the patient.

Lasix is a stress test that kills.

We should listen to Dr. Wesley and stop killing our patients.

What should we use?

NTG (NiTroGlycerin – GTN GlycerylTriNitrate in Commonwealth countries) does the opposite of what Lasix does. Higher doses of NTG produce better outcomes.
 

Also read NTG and the Hero Medic at Street Watch: Notes of a Paramedic, for a perspective on high dose NTG for acute CHF.

Would half a bottle of NTG tabs kill an acute CHF patient? No, and that is still much safer than giving Lasix to acute CHF patients.
 
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Footnotes:

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[1] Lasix Kills: Better Therapy for CHF<
Nov 2 2012 8:00AM
Room: 217
Category: ALS
Keith Wesley, MD, FACEP
Conference schedule for Friday.

This lecture examines our better understanding of the pathophysiology of congestive heart failure and the history of its treatment. Old theories result in old therapies, and current research should guide us in providing better prehospital therapy for this deadly condition. We will explore the role of pharmacologic agents such as diuretics and nitrates, as well as the value of continuous positive airway pressure (CPAP) support.

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[2] 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.

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[3] Acute vasoconstrictor response to intravenous furosemide in patients with chronic congestive heart failure. Activation of the neurohumoral axis.
Francis GS, Siegel RM, Goldsmith SR, Olivari MT, Levine TB, Cohn JN.
Ann Intern Med. 1985 Jul;103(1):1-6.
PMID: 2860833 [PubMed – indexed for MEDLINE]

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[4] Nitroglycerin for Treatment of Acute, Hypertensive Heart Failure – Bolus, Drip or Both?
Wed, 17 Oct 2012
Rogue Medic
Article with links to plenty of studies on high dose NTG

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Filed Under: CPAP, EMS Expo, Heresy, Lasix, NTG, Pharmacology, Research

EMS NTG for CHF – Bolus or Infusion – Part II

Wed, 12 Oct 2011 06:30:39 -0400 by
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Continued from Part I.

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This continues my response to Too Old To Work, Too Young To Retire’s response to A Comment on Saving Patients from Low Doses of NTG.

I’d love to be able to do IV NTG in the field, but can’t seem to get our medical director interested in it. That might be because someone else has to approve the purchase of the pumps. It sure would help patients, though.

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This is the biggest problem with treating CHF with IV NTG. There are too many doctors, nurses, medics, et cetera who just do not understand. They think that too much NTG is the problem, but the opposite is true. We are killing patients by not giving them enough NTG.

Where has any danger of too much IV NTG been demonstrated?

Competent people will decrease the rate of administration if there are significant drops in blood pressure. Therefore, complications do not ensue.

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From 1984 through 1991, new guidelines for the use of intravenous nitrates, based on differential treatment according to blood pressure, were in use.

RESULTS:
Overall prehospital mortality rate for APE in all patients was 7.8% (50 of of 640 patients). Mortality after 1984 was significantly lower than before (5.3% versus 13%, P < .01). Nitrates were effective in reducing mortality, even in hypotensive patients. Multivariate analysis showed that outcome was significantly affected by two clinical features (dyspnea and low blood pressure), treatment with nitrates, and calendar period effects (before/after 1984).[1]

Not just hypertensive patients, but also hypotensive patients benefited from EMS IV NTG!

Nitrates were effective in reducing mortality, even in hypotensive patients.

The CHF death rate dropped from 13% all the way down to 5.3%

 

Without prehospital IV NTG the death rate was 2 1/2 times higher.

 

2 1/2 times as much death is not a subtle difference.

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Picture credit.

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No. We should skip the pump and use something faster – something that works just as well for EMS.

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The big question – Is any infusion pump needed?

No.

Absolutely not.

administered repeated boluses of nitroglycerin.[2]

Just one or two repeated boluses of NTG?

The mean number of nitroglycerin boluses required was 4, [2]

But the IV NTG boluses must have been low doses.

a mean dose of 1588 mcg (range 800-28,000 mcg).[2]

0.8 mg to 28 mg – not small doses of IV NTG.

Two patients had transitory dips in SBP < 100, which resolved spontaneously; both of these patients received additional nitroglycerin boluses.[2]

The deadly hypotension got better on its own.

So much for the extreme danger of too much NTG.

None (0%) of the patients required intubation (95% CI 0-7.3%).[2]

Avoiding intubation saves lives.

Prehospital NTG can should be done with IV boluses.

No pumps required.

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We are already using NTG bolus treatment, so we should accept that IV boluses of NTG are not that much different from SL (SubLingual) boluses. If we push 1 mg NTG at a time, that is only the dose equivalent of two and a half NTG tabs. More is absorbed than with SL, but this is still not really a large dose.

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Footnotes:

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[1] Intravenous nitrates in the prehospital management of acute pulmonary edema.
Bertini G, Giglioli C, Biggeri A, Margheri M, Simonetti I, Sica ML, Russo L, Gensini G.
Ann Emerg Med. 1997 Oct;30(4):493-9.
PMID: 9326864 [PubMed – indexed for MEDLINE]

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[2] A Protocol of Bolus-Dose Nitroglycerin and Non-Invasive Ventilation to Avert Intubation in Emergency Department Acute Pulmonary Edema
Piyush Mallick, Surjya Upadhyay, TS Senthilnathan, El Matit Waleed , Al Jahra Hospital, Scott Weingart, Mount Sinai School of Medicine
Prepublication abstract
PDF Download of page at EMCrit

EMCrit Podcast 1-Sympathetic Crashing Acute Pulmonary Edema
by EMCRIT on APRIL 25, 2009
Link to Podcast page

Link to page with other evidence supporting this treatment

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Filed Under: CPAP, Heresy, Intubation, NTG, Pharmacology

EMS NTG for CHF – Bolus or Infusion – Part I

Tue, 11 Oct 2011 06:30:47 -0400 by
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In response to A Comment on Saving Patients from Low Doses of NTG, there is the following comment from Too Old To Work, Too Young To Retire.

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Intubation, with or without RSI is far riskier for the patient. Not to mention that it lengthens ICU stays, has the risk of VAP, and lastly drives up costs. It’s the VAP that’s the killer, sometime literally.

Abbreviations used are listed in the footnotes.[1]

This is the most important difference between intubation (Invasive Positive Pressure Ventilation) and CPAP (NIPPV = Non-Invasive Positive Ventilation). Invasive airways lead to pneumonia.

The attributable morbidity and mortality of VAP are clinically important. In a prospective, matched cohort study, patients with VAP remained in the ICU 4.3 days (95% CI, 1.5 to 7.0 days) longer than patients who did not have VAP and had a trend toward an increased risk for death (absolute risk increase, 5.8% [CI, 2.4% to 14.0%]) (14). Six other studies using a matching strategy found a prolonged length of ICU stay associated with VAP (range, 5 to 13 days) and attributable mortality ranging from an absolute risk increase of 0% to 50% (15–20).[2]

Longer ICU stays and increased risk of death with intubation. What if they looked exclusively at patients intubated by EMS? How much longer would the ICU stays be? How much higher would the risk of death be?

Avoiding intubation is important.

CPAP helps to avoid intubation.

High dose NTG helps to avoid intubation.

Furosemide (Lasix) does not.

What should we use? CPAP and high-dose NTG.

What should we avoid? Intubation and Lasix.

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We don’t see intubation in the hospitals for CHF patients very frequently. In fact, they were ahead of us on using CPAP by several years. That angered a lot of the medics because we knew that there was a better way to treat patients.

We still do not use treatment that is aggressive enough.

This is just one of the ways that people kill patients with – You can’t be too careful.

We have been too carefully killing patients.

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I’d love to be able to do IV NTG in the field, but can’t seem to get our medical director interested in it. That might be because someone else has to approve the purchase of the pumps. It sure would help patients, though.

Here are some comments from someone concerned about the use of IV NTG by EMS without pumps –

It is generally agreed in the literature that for intravenous administration, the initial dosage should be set to 5 mg/min and this dose increased by 5 mg/min every 5 minutes until the desired effect is achieved or systolic blood pressure decreases below 100 mm Hg or a dose of 200 mg/min is attained.2[3]

This dose is not just too low, but this dose is so low that it will kill patients.

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The median time of application was 12 minutes (range 4 to 33 minutes), and median applied nitroglycerin dose was 68 mg/min (range 35 to 255 mg/min). We concluded that nitroglycerin was excessively overdosed in regard to time of therapy.[3]

These doses are probably still too low.

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Presumably severe clinical consequences were prevented only by the relatively short ambulance time in an urban setting.[3]

Here is one problem with this comment – there is no reference to any adverse effect from the higher than usual doses of NTG.

Why?

Because these doctors have probably been killing patients by not giving hypertensive CHF patients enough NTG.

If the NTG were dangerous, they would have seen adverse events in patients receiving NTG for periods much longer than the effect of NTG. NTG wears off very quickly, so 10 minutes or 20 minutes would be plenty long enough to kill patients, but these NTG doses were not excessive, even though these doses scared the doctors.

Too much fear.

Plus

Not enough understanding of medicine.

Equals

Dead patients from inadequate doses of NTG.

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To be completed in Part II.

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Footnotes:

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[1] Abbreviations
RSI = Rapid Sequence Induction/Intubation
VAP = Ventilator-Associated Pneumonia
CPAP = Continuous Positive Airway Pressure
NIPPV = Non-Invasive Positive Ventilation
NTG = NiTroGlycerin (in Commonwealth countries, GTN + GlycerylTriNitrate)
IV = IntraVenous
SL = SubLingual

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[2] Evidence-based clinical practice guideline for the prevention of ventilator-associated pneumonia.
Dodek P, Keenan S, Cook D, Heyland D, Jacka M, Hand L, Muscedere J, Foster D, Mehta N, Hall R, Brun-Buisson C; Canadian Critical Care Trials Group; Canadian Critical Care Society.
Ann Intern Med. 2004 Aug 17;141(4):305-13.
PMID: 15313747 [PubMed – indexed for MEDLINE]

Free Full Text from Annals of Internal Medicine

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[3] Preclinical intravenous nitroglycerin therapy.
Roeggla G, Hauser I, Wagner A, Roeggla M.
Ann Emerg Med. 1998 Mar;31(3):416. No abstract available.
PMID: 9506507 [PubMed – indexed for MEDLINE]

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Filed Under: CPAP, Heresy, Intubation, NTG, Pharmacology

A Spoken DNR – Should EMS Honor It?

Sun, 09 Mar 2008 04:15:00 -0400 by
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In the March 2008 EMS Magazine there is an article by James J. Augustine, MD, FACEP. The title is Don’t Put That Tube In!

The article is about CPAP, which is an important topic and an excellent treatment that isn’t used anywhere near enough.

The patient is speaking and EMS is having trouble hearing her.The crew looks up at him. “Don’t put the tube in,” he reiterates. “She’s been on the machine before, and she doesn’t want that ever again. The tube means the machine, and neither of us will agree to that. Don’t put the tube in.”

That makes it fairly clear.[1]

Well, I may be a little slow, but to me that does not make the role of EMS fairly clear. I wish it did and I believe it should, but I’ve been in EMS too long to not see this as leading to a free for all of ethical, spiritual, legal, procedural, political, and administrative Monday morning quarterbacks sharpening their claws in preparation for a nice juicy sacrificial lamb, or two.

In the article the treatments help avoid intubation, but what if the patient progresses to respiratory failure?

How many EMS providers are permitted by state EMS law to observe such a patient’s spoken demand, even when accompanied by the backing of a family member?

If there is a DNR and the DNR is not the original prehospital DNR specifying no intubation, or if a family member disagrees with honoring the jumped through all of the hoops to be allowed to die outside of the hospital DNR, or any of the other possibilities that lead to this being far from clear.

Yes, the trained Protocol Monkey[2] will see that the best way to not get in trouble is to follow the protocols: I’m sorry, this is a standard DNR – not a prehospital DNR. I may not follow its clear documentation of your wishes, of your informed refusal of treatment. The state EMS laws absolve me of any responsibility for my actions when I violate a DNR.

Or PM may decide to call medical command to obtain orders to follow the valid legal document that was completed in good faith. If the patient is determined to need one of those treatments that the DNR refuses, the PM is obligated to provide the treatment while attempting to contact medical command, because What if medical command says to treat the patient against the patient’s wishes, for whatever reason?

Or PM laughs at the suggestion that a respiratory distress patient has the capacity to make informed decisions about care that the patient is very familiar with – much more so than the PM. The patient has got to be hypoxic to not want a prehospital non-RSI tube.

Or the responding EMS crew is a PM-free zone on that call and doesn’t automatically follow the state-approved Just Say No To DNR’s policy?

This is just assuming the policies of the state I am most familiar with. It may not be representative of other states. Maybe you live in a state that encourages its medics to use their own judgement, provides them with good initial training/continuing education to prepare for using that judgement, and aggressively follows up on cases where judgement is exercised.

So, given the many possibilities, how do you think you would act?

Use the case from the article or an example of your own.

I am interested in what people think about this, because I obviously do not see this conundrum as one that is set up to benefit the patient.

Why are we doing all of this, if not for the benefit of the patient?

Forcing a tube down the airway of a patient who does not want it, maybe to feel that we have given it our all, seems very wrong to me.

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Footnotes:

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[1] Don’t Put That Tube In!
EMS Magazine EMS World
March 2008
by James J. Augustine, MD, FACEP.
Article

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[2] Protocol Monkey is borrowed from Ambulance Driver’s bestiary and has the uncanny ability to replicate itself faster than bacteria, is disposable, possesses a pulse, and has a medic card – what more could you possibly want in patient care?

Updated formatting and links 10-27-10 – 22:23
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Filed Under: CPAP, DNR, EMS Magazine, Ethics, Heresy