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

- Rogue Medic

The Art of Critical Thinking at The EMS Roundtable


Last night I called in to the EMS Roundtable because the topic was one of the most important in EMS – critical thinking.[1]

Critical thinking is the intellectually disciplined process of actively and skillfully conceptualizing, applying, analyzing, synthesizing, and/or evaluating information gathered from, or generated by, observation, experience, reflection, reasoning, or communication, as a guide to belief and action.[2]


More simply, in EMS critical thinking is how we make good decisions based on the limited information available in the emergency setting.

In EMS we definitely can be too safe.

Not applying a tourniquet, because What if the tourniquet causes a problem?

That is being too safe.

Not giving large doses of NTG to a hypertensive CHF patient, because What if the NTG causes the pressure to bottom?

That is being too safe.

Strapping someone to a backboard with straps and a collar, Just to be safe.

How is that not being too safe?

Where is there any evidence that spinal immobilization is safe?

Not sedating (or not adequately sedating) an excited delirium patient, because What if he stops hyperventilating?

That is being too safe.

These are some of the things that need to be considered when we engage in critical thinking.

Go listen to the podcast.

Show Notes:

Guest Dan Limmer: http://limmercreative.com

Live Call-in Tim Noonan: http://roguemedic.com

Chat Room:

Jim Hoffman: http://emsofficehours.com

Tom Bouthillet: http://EMS12Lead.com


Go listen to the podcast.


[1] The Art of Critical Thinking
The EMS Roundtable
Wed, April 24, 2013 07:00 pm
Podcast page.

[2] Defining Critical Thinking
Web page


Is Nitroglycerin Bad for Severe Sepsis?


Yesterday at The Paramedic’s Edge, this was the topic of reactive, reflexive, dogmatic, rejection discussion of a possible use of NTG (NiTroGlycerin – GTN GlycerylTriNitrate in Commonwealth countries).

NTG is a vasodilator and sepsis is a vasodialtion problem. There are other problems with sepsis, but vasodilation may be the primary problem.

Nitro for severe septic patients. What are your thoughts?[1]


Here is a sampling of some of the unfortunately typical responses.

The amateur lawyer who thinks that what we do should be guided by fear of law suits approach.

Oh to put them out of their misery?! Sounds like a lawsuit waiting to happen


The just drive fast, I don’t understand any of this medical mumbo jumbo appraoch.

We’re medics not doctors. Best thing we can do is a diesel infusion


The most common responses seemed to be of this kind.

The I only know one thing about nitro and that scares me approach.

True hemodynamic instability is a contraindication


Hmmmm let’s drop their pressure even more…that’s a thought? So my answer…HE’LL NO!!


We will probably end up using NTG in the treatment of cardiac arrest – the ultimate low blood pressure state, so how far fetched is using NTG for sepsis?[2],[3],[4],[5],[6],[7]


NTG can lower blood pressure, but it can also increase cardiac output.

To over-simplify things –

If the CO (Cardiac Output) increases by more than the the vasodilation would decrease the BP (Blood Pressure), the BP will actually be expected to increase.

CO = SV (Stroke Volume) x HR (Heart Rate).

CO MAP (Mean Arterial Pressure)/TPR (Total Peripheral Resistance).

BP = CO x TPR.

Are all cardiac outputs and vascular resistances the same? No, but we simplify things by making that assumption.


Jean-Charles Preiser and colleagues question the routine use of nitroglycerin because of the risk of hypotension and the possible induction of mitochondrial dysfunction.[8]


Many people question the use of NTG and worry about hypotension.

Although we observed a temporary drop in blood pressure, blood flow was maintained and, in fact, increased in our patients.[8]


We do worry obsess about things that are brief and insignificant (such as ROSC – Return Of Spontaneous Circulation – in treatment of cardiac arrest), while we ignore the things that are more important (such as living long enough to leave the hospital with a brain that works well enough to recognize family members).

Space constraints meant that we were not able to include specific haemodynamic results in our Research letter, but mean arterial pressure temporarily dropped by an average of 21 mm Hg (range 13—33 mm Hg) in the eight patients we investigated.[8]


A drop in MAP (Mean Arterial Pressure) of 21 mm/Hg is huge!

Mean arterial pressure returned to baseline level within 1 min in all patients with concomitant fluid infusion.[8]


Less than 1 minute?

Try using that as a pickup line.

I can rock your world for less than 1 minute.

How much alcohol is going to be required to make that sound significant?

We give adenosine to do what?

To completely stop the heart for usually less than one minute.

We cardiovert to do what?

To completely stop the heart for usually less than one minute.

A short-term worsening of vital signs for a long-term improvement in survival is an excellent trade-off.

Does NTG improve long-term survival?

That is not clear, but this does show that we need to abandon more dogma in our search for the best care of our patients.

The increase in microvascular blood flow as a result of this procedure confirms our clinical experience that resuscitation efforts should be aimed at optimising blood flow not blood pressure.[8]


NTG does improve blood flow.

Too many of us are afraid to use NTG, or afraid to use large doses of NTG, or afraid to use IV bolus NTG, or afraid to use large doses of IV bolus NTG out of too much concern for blood pressure and not enough concern for blood flow.

This quotes are from a response to a letter about research paper looking at NTG for sepsis. This paper is not something that should be summarily dismissed.[9]

The EMS drug of choice, dopamine, may be a bad idea for sepsis.[10],[11]

Think about that – For sepsis dopamine may make things worse and NTG may make things better.

Is it that simple? Maybe. Maybe not. Dopamine may make things better, but just not do as good a job as norepinephrine. Or all catecholamines may be harmful.

Dr. Mervyn Singer makes an excellent case that catecholamines are not helpful, or that they are at least tremendously overused. Go listen to his podcast.[12]


[1] Nitro for severe septic patients. What are your thoughts?
The Paramedic’s Edge
Facebook discussion page

[2] High dose nitroglycerin treatment in a patient with cardiac arrest: a case report.
Guglin M, Postler G.
J Med Case Rep. 2009 Aug 10;3:8782. doi: 10.4076/1752-1947-3-8782.
PMID: 19830240 [PubMed]

Free Full Text from PubMed Central.

A possible explanation for the hemodynamic benefit of NTG in our patients is increased cardiac output produced by rapid vasodilatation in a heart operating at the extreme of the Frank-Starling curve. Vasodilators in heart failure with or without acute myocardial infarction have been proven to decrease left ventricular filling pressure and systemic vascular resistance while increasing cardiac index [7]. The more severe the failure, the more beneficial the effect of vasodilators [13].

[3] Sodium nitroprusside enhanced cardiopulmonary resuscitation improves survival with good neurological function in a porcine model of prolonged cardiac arrest.
Yannopoulos D, Matsuura T, Schultz J, Rudser K, Halperin HR, Lurie KG.
Crit Care Med. 2011 Jun;39(6):1269-74. doi: 10.1097/CCM.0b013e31820ed8a6.
PMID: 21358401 [PubMed – indexed for MEDLINE]

Free Full Text from acoep.org.

[4] Sodium nitroprusside-enhanced cardiopulmonary resuscitation improves resuscitation rates after prolonged untreated cardiac arrest in two porcine models.
Schultz JC, Segal N, Caldwell E, Kolbeck J, McKnite S, Lebedoff N, Zviman M, Aufderheide TP, Yannopoulos D.
Crit Care Med. 2011 Dec;39(12):2705-10. doi: 10.1097/CCM.0b013e31822668ba.
PMID: 21725236 [PubMed – indexed for MEDLINE]

Free Full Text from PubMed Central.

[5] Sodium nitroprusside enhanced cardiopulmonary resuscitation (SNPeCPR) improves vital organ perfusion pressures and carotid blood flow in a porcine model of cardiac arrest.
Schultz J, Segal N, Kolbeck J, McKnite S, Caldwell E, Yannopoulos D.
Resuscitation. 2012 Mar;83(3):374-7. doi: 10.1016/j.resuscitation.2011.07.038. Epub 2011 Aug 22.
PMID: 21864483 [PubMed – indexed for MEDLINE]

Free Full Text from PubMed Central.

[6] Sodium nitroprusside enhanced cardiopulmonary resuscitation prevents post-resuscitation left ventricular dysfunction and improves 24-hour survival and neurological function in a porcine model of prolonged untreated ventricular fibrillation.
Schultz J, Segal N, Kolbeck J, Caldwell E, Thorsgard M, McKnite S, Aufderheide TP, Lurie KG, Yannopoulos D.
Resuscitation. 2011 Dec;82 Suppl 2:S35-40. doi: 10.1016/S0300-9572(11)70149-6.
PMID: 22208176 [PubMed – indexed for MEDLINE]

[7] Controlled pauses at the initiation of sodium nitroprusside-enhanced cardiopulmonary resuscitation facilitate neurological and cardiac recovery after 15 mins of untreated ventricular fibrillation.
Yannopoulos D, Segal N, McKnite S, Aufderheide TP, Lurie KG.
Crit Care Med. 2012 May;40(5):1562-9. doi: 10.1097/CCM.0b013e31823e9f78.
PMID: 22430233 [PubMed – indexed for MEDLINE]

[8] Nitroglycerin for septic shock.
Preiser JC, De Backer D, Vincent JL.
Lancet. 2003 Mar 8;361(9360):880; author reply 880. No abstract available.
PMID: 12642079 [PubMed – indexed for MEDLINE]

Free Full Text from the Lancet.

[9] Nitroglycerin in septic shock after intravascular volume resuscitation.
Spronk PE, Ince C, Gardien MJ, Mathura KR, Oudemans-van Straaten HM, Zandstra DF.
Lancet. 2002 Nov 2;360(9343):1395-6.
PMID: 12423989 [PubMed – indexed for MEDLINE]

[10] Dopamine versus norepinephrine in the treatment of septic shock: a meta-analysis*.
De Backer D, Aldecoa C, Njimi H, Vincent JL.
Crit Care Med. 2012 Mar;40(3):725-30. doi: 10.1097/CCM.0b013e31823778ee.
PMID: 22036860 [PubMed – indexed for MEDLINE]

In patients with septic shock, dopamine administration is associated with greater mortality and a higher incidence of arrhythmic events compared to norepinephrine administration.

[11] Norepinephrine or dopamine for septic shock: systematic review of randomized clinical trials.
Vasu TS, Cavallazzi R, Hirani A, Kaplan G, Leiby B, Marik PE.
J Intensive Care Med. 2012 May-Jun;27(3):172-8. doi: 10.1177/0885066610396312. Epub 2011 Mar 24. Review.
PMID: 21436167 [PubMed – indexed for MEDLINE]

The analysis of the pooled studies that included a critically ill population with shock predominantly secondary to sepsis showed superiority of norepinephrine over dopamine for in-hospital or 28-day mortality.

[12] Catecholamines Should Be Banned
Mervyn Singer
6th Annual Critical Care Symposium
Manchester, UK
Page with link to free mp3 download from Free Emergency Medicine Talks.

Guglin, M., & Postler, G. (2009). High dose nitroglycerin treatment in a patient with cardiac arrest: a case report Journal of Medical Case Reports, 3 (1) DOI: 10.4076/1752-1947-3-8782

SPRONK, P., INCE, C., GARDIEN, M., MATHURA, K., & ZANDSTRA, D. (2003). Nitroglycerin for septic shock The Lancet, 361 (9360), 880-880 DOI: 10.1016/S0140-6736(03)12692-X

Spronk, P., Ince, C., Gardien, M., Mathura, K., Straaten, H., & Zandstra, D. (2002). Nitroglycerin in septic shock after intravascular volume resuscitation The Lancet, 360 (9343), 1395-1396 DOI: 10.1016/S0140-6736(02)11393-6


Does an Oxygen Saturation of 100% Mean an Overdose?


Are we harming patients with oxygen?[1]

This will offend many in the oxygen religion, but we should start thinking of oxygen overdose.

What is our use of oxygen for everything based on?

Received wisdom from authority figures. We need to stop using authority and tradition as excuses to harm people.

Tom Bouthillet, Kelly Arashin, and Mike McEvoy discuss the harms of oxygen and the evidence of harm.

Go listen to the podcast, or watch the video.

Then reconsider your answer to my question.

Are we overdosing our patients, when we raise their oxygen saturation to 100%?

What if the original oxygen saturation was 94%?

What if the original oxygen saturation was 74%?

What if the original oxygen saturation was 54%?

Does the original oxygen saturation matter?

Would we have the same worries if the drug (oxygen is a drug) is morphine, NTG, midazolam, or even amiodarone?

Why do we grant the beliefs of the religion of oxygen such immunity from examination?


According to Mike McEvoy, the goal is 92% to 96%.

Not 97%.

98% is worse.

99% is much worse.

100% is as bad as it can get – even worse than hypoxia.


Go listen to the podcast, or watch the video.

A couple of points. Mike McEvoy states that the intensive care community has been familiar with this since the 1990s. This has been studied, and there has been evidence of harm since at least as early as 1950.

The administration of 100 per cent oxygen may actually be contraindicated in patients in whom oxygen saturation of arterial blood is normal.[2]


This was a decade before we found out that internal mammary artery ligation is nothing more than a placebo surgery.[3] That extremely popular procedure was done away with so quickly, that few people even remember the use of internal mammary artery ligation as a treatment for angina?

Oxygen has tradition behind it encouraging us to keep killing patients.

We should have been smart enough to reconsider our devotion to received wisdom and authority in 1950.

Many of us still refuse to learn.

This is why we need evidence before applying treatments to everyone.

How many hundreds of thousands of patient have we killed with oxygen and our refusal to require evidence of improved outcomes?


Go listen to the podcast, or watch the video.


[1] EMS 12-Lead podcast – Episode #11 – Are we harming patients with oxygen?
EMS 12 Lead Podcast
EMS 12 Lead
Page with podcast and video podcast.

[2] One hundred percent oxygen in the treatment of acute myocardial infarction and severe angina pectoris.
J Am Med Assoc. 1950 Sep 30;144(5):373-5. No abstract available.
PMID: 14774103 [PubMed – indexed for MEDLINE]

In five patients with angina pectoris the administration of 100 per cent oxygen did not favorably influence the onset or duration of pain or the electrocardiographic alterations induced by standard exercise. On the contrary, oxygen therapy actually appeared responsible for more pronounced and persistent electrocardiographic changes in several patients.

[3] An evaluation of internal-mammary-artery ligation by a double-blind technic.
N Engl J Med. 1959 May 28;260(22):1115-8. No abstract available.
PMID: 13657350 [PubMed – indexed for MEDLINE]


Worst test question ever! – Maybe


Thank you to David Baumrind of EMS 12 Lead for linking to this here. It probably is not the worst test question ever, but it is very bad.

Read the question, figure out what your response would be, then scroll down for my explanation.

You are dispatched emergency traffic to the scene of a 24 yo F with “palpitations.” You arrive to find her pale, sweaty and lethargic. You palpate a radial pulse with an extreme rate. You hook her up to the monitor and find the following rhythm? You have a 45 minute transport time. Which of the following is the most appropriate initial treatment for this condition?

1.) Nitroglycerin 0.4mg SL
2.) Immediate synchronized cardioversion
3.) Adenosine 12mg Rapid IV push followed by 20cc NS bolus
4.) Epinephrine 1mg 1:10000 q-3-5m IVP

-Admin Paul

The original posting was from Exhausted Medic Students ‘R’ Us here.

Go read the original with its hundreds of comments.
























All of the answers are completely wrong.

ST (Sinus Tachycardia) is the rhythm.

There are clear P waves with consistent PR intervals. It is faster than what some people expect to see from ST, but that is because many of us do not think about what we are learning in EMS.

It is true that the cardiology part of paramedic school is probably the toughest for most people, and we are overwhelmed with new information, but we should be very familiar with this rhythm.

Carry a patient up/down a flight of steps and you may have significant ST – maybe even faster than what is on this strip. If your heart rate is over 150, so what?

Before you have a chance to recover, use the pulse oximeter to measure your heart rate after carrying a patient. You are just checking the accuracy of the machine before applying it to the patient, or before reconnecting it to the patient.

1. Nitroglycerin is NOT indicated for palpitations.

NTG is not indicated even for a lot of palpitations. Do you have a protocol for NTG for palpitations?

Ask your medical director how much NTG should be given for palpitations, but don’t be surprised if you are expected to go through some scenarios to demonstrate that you would not really give NTG for palpitations.

2. Cardioversion is NOT indicated for sinus tachycardia.

Cardioversion is supposed to cause asystole. During that asystole, it is hoped that the sinus node will become the pacemaker for the patient’s rhythm.

SINUS tachycardia means that the sinus node is already the pacemaker.

Cardioversion of sinus tachycardia can only make things worse.

Cardioversion of sinus bradycardia can only make things worse.

Cardioversion of any sinus rhythm can only make things worse.

3. Adenosine is NOT indicated for sinus tachycardia.

The dose does not matter. The drug is not indicated.

No matter how wrong NTG is for palpitations, adenosine is worse.

4. Epinephrine is NOT indicated for sinus tachycardia with a pulse.

How much faster do we want this ST to be? Epinephrine can make it faster.

Maybe some people think that the choices should include a vagal maneuver.

No. That would also be wrong.

Calcium channel blocker?

Another wrong.

Beta blocker?

Wrong again.

No competent paramedic should attempt to justify any of these answers.

Maybe this is a question to find out just how incompetent people will be to satisfy an authority figure.

One horrible answer is –

As a paramedic instructor and a evaluator for National Registry…if my student didn’t cardiovert…I’m failing them.


Does the National Registry hire people this ignorant as evaluators?

Yes, but so does every other testing organization. Maybe this guy is lying about being an instructor and evaluator, but this is EMS and we like low standards.

A defender of cardioversion posted the ACLS tachycardia cheat sheet.

Click on image to make it larger.


Unfortunately, the cheat sheet does not state that we should not shock sinus tachycardia.

If all we know is the cheat sheet, we should consider a career change to explore the exciting world of fast food order fulfillment.

The text of the 2010 ACLS guidelines states –

ACLS professionals should be able to recognize and differentiate between sinus tachycardia, narrow-complex supraventricular tachycardia (SVT), and wide-complex tachycardia.[1]


A lot of people could not recognize an obvious sinus tachycardia.

Is that the fault of their instructors?

Yes and No.

Sinus tachycardia is among the rhythms listed that we are expected to be able to identify.

Synchronized cardioversion is recommended to treat (1) unstable SVT, (2) unstable atrial fibrillation, (3) unstable atrial flutter, and (4) unstable monomorphic (regular) VT. Shock can terminate these tachyarrhythmias by interrupting the underlying reentrant pathway that is responsible for them.[1]


Sinus tachycardia is not listed among the rhythms that should be shocked.

Here is the important part –

If judged to be sinus tachycardia, no specific drug treatment is required. Instead, therapy is directed toward identification and treatment of the underlying cause. When cardiac function is poor, cardiac output can be dependent on a rapid heart rate. In such compensatory tachycardias, stroke volume is limited, so “normalizing” the heart rate can be detrimental.[1]


We treat sinus tachycardia by treating the cause.

The cause of sinus tachycardia is never lack of cardioversion.

A good test near the end of the cardiology section of paramedic school might include this question to find out if the students have learned anything.

All of the choices are wrong.

In medicine, there is not one best answer for all patients.

Anyone who says differently is selling something.


[1] Tachycardia
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 8: Adult Advanced Cardiovascular Life Support
Part 8.3: Management of Symptomatic Bradycardia and Tachycardia
Cardioversion and Regular Narrow-Complex Tachycardia


Is a half a bottle of nitro too much for a single dose?

In what I last wrote about the emergency treatment of CHF (Congestive Heart Failure) and furosemide (Lasix – frusemide in Commonwealth countries) being a bad drug,[1] I also mentioned what Peter Canning had written about Hero Medic and a very high dose of NTG (NiTroGlycerin – GTN GlycerylTriNitrate in Commonwealth countries).

How much NTG?

The hero medic opened the nitro, pulled open the patient’s mouth and poured in what seemed like half the container. The hero medic closed the patient’s mouth, and then told the new medic. “You should be all set.”[2]


What seemed like half the container of something we are warned not to give chest pain patients more than one at a time and never more than 3 tabs of – ever!

That does seem like a lot, but how much is half of a bottle?


How much is a lot?


For the typical bottle pictured, the label states that the total is 25 of the 0.4 mg tabs.

That is a total of 10 mg. Half of that is easy math – 5 mg.

What seemed like half the container is probably less than half, but it was just such a shocking visual for the narrator, that all he could do was estimate.

Is 5 mg a large dose?


Is 5 mg a dangerous dose?

That depends on the patient presentation.

a patient in severe pulmonary edema who was circling the drain[2]


I would like to know his blood pressure, but even hypotensive CHF patients do well with huge doses of NTG.

The patients below were more than just circling the drain.

All were hypotensive, or pulseless.

Click on the image to make it larger.[3]


Almost all of the massive dose NTG patients survived.

The highest blood pressure before NTG was 80/70.

The lowest dose of NTG was 1 mg – and that was the only patient who received less than 5 mg NTG.

Almost every hypotensive patient received much more than 5 mg NTG.

Is 5 mg NTG a dangerous dose?

Probably not.

Is 5 mg a scary dose?

Of course. We have been trained to be scared of NTG.

That dose is just much larger than most people are comfortable with, because of fear and inexperience.

You can talk about the hero medic acting off protocol and being a cowboy, etc, but the story still resonates for me.[2]


Would it be appropriate to just drop in, give a large dose of anything, and then not stick around?

No. If the original medic is not comfortable with that treatment, the Hero Medic should be there to hold the nitrophobic medic’s hand and reassure the medic to follow his assessment, rather than to follow his anxiety. That is the way we learn.

The story of Hero Medic is told through hyperbole – exaggeration to make an important point.

I have done this with others. Look, not only am I giving a much larger dose than you claim is safe – I am going to add a few more tabs – just to make a point.

If the scare stories about NTG were true, the patients would bottom out their blood pressures, but it is only the witnesses who bottom out their blood pressures, due to over-stimulation of their vagal nerves. The patients improve.

Some people learn from this clear demonstration that they have been lied to, but others choose to believe the dogma even after seeing clear evidence that the dogma is a lie.

Doctors, nurses, medics, et cetera. They are equally susceptible to dogma.

Is the Hero Medic a cowboy?

No, the Hero Medic s a teacher.

We need to be smart enough to learn.


[1] Lasix Kills: Better Therapy for CHF
Wed, 07 Nov
Rogue Medic

[2] NTG and the Hero Medic
Street Watch
November 7, 2012

[3] High dose nitroglycerin treatment in a patient with cardiac arrest: a case report.
Guglin M, Postler G.
J Med Case Reports. 2009 Aug 10;3:8782.
PMID: 19830240 [PubMed]

Free Full Text from PubMed Central


Lasix Kills: Better Therapy for CHF

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?


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]



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.


[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.

[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.

[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]

[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


Nitroglycerin for Treatment of Acute, Hypertensive Heart Failure – Bolus, Drip or Both?


If standard doses of nitrate – NTG (NiTroGlycerin – GTN GlycerylTriNitrate in Commonwealth countries), ISDN (IsoSorbide DiNitrate), or ISMN (IsoSorbide MonoNitrate) improve outcomes for CHF/ADHF (Congestive Heart Failure/Acute Decompensated Heart Failure) patients, and larger IV (IntraVenous) doses are more effective than standard doses,[1],[2],[3],[4],[5],[6],[7],[8],[9],[10],[11],[12] what method(s) of drug delivery works best?

High dose IV drip?

High dose IV bolus?

A high dose IV bolus combined with a high dose IV drip?

We performed a retrospective cohort study of patients who presented to the emergency department (ED) of an urban, teaching hospital with severe, acute hypertensive heart failure between Jan 2007 and July 2011 and received intravenous nitroglycerin. 3 subgroups were defined: 1) those given nitroglycerin by higher dose (≥ 0.5 mg) bolus alone (higher dose nitroglycerin); 2) those given nitroglycerin by continuous intravenous infusion alone (intravenous nitroglycerin); and 3) those given nitroglycerin by concurrent higher dose bolus and continuous IV infusion (higher dose intravenous nitroglycerin).[13]


At least half a milligram at a time means at least 25% more than the standard bolus dose with a NTG tab/spray.


Click on images to make them larger.

With bolus dosing the blood pressure dropped more quickly.

The sooner we drop the patient’s blood pressure, as long as we do not drop it too much, the better for the patient.

Do we really have a problem with dropping the pressure too much with high doses of bolus IV NTG?


Almost every severely hypotensive patient in this study received more than 1 mg/minute IV NTG, which would be boluses of at least 5 mg IV NTG every 5 minutes until they improved – and most did improve dramatically.[14]



Conclusion: In this single-center, retrospective, unadjusted analysis of primarily African-American patients with acute hypertensive heart failure, nitroglycerin administered by higher dose bolus without concurrent intravenous infusion was associated with a significant decrease in ICU admissions and hospital length of stay. Based on our findings, bolus higher dose nitroglycerin appears to be a viable option for the management of such patients.[13]


There are some important questions about IV bolus dosing of NTG for CHF/ADHF.

How aggressive should our initial bolus dose be?

How often should we repeat the dosing?

NTG is metabolized very quickly, so these boluses are only to treat the initial emergency, then the patient will be switched to an infusion of NTG.

We do need more research, but we also need research that does not include furosemide, or compares furosemide with a placebo.

This evidence is much better than any evidence used to justify epinephrine in cardiac arrest. If any CHF/ADHF patients have a cardiac arrest and they are not immediately resuscitated, they are supposed to be treated with epinephrine according to the current ACLS (Advanced Cardiac Life Support) guidelines.

These patients do not arrest due to any deficiency of adrenaline (epinephrine).

These patients improve with treatment that is essentially the opposite of epinephrine.


[1] [The efficacy of isosorbide dinitrate administered in an intravenous bolus in acute cardiogenic pulmonary edema].
Rabaçal C, Ribeiro H, Nuno L, Mendonça C, Linder J, Pereira D, Carvalho E, Afonso JS, Fernandes JS.
Rev Port Cardiol. 1993 Dec;12(12):1029-35, 1000. Portuguese.
PMID: 8117456 [PubMed – indexed for MEDLINE]

[2] Intravenous nitroglycerin boluses in treating patients with cardiogenic pulmonary edema.
Nashed AH, Allegra JR.
Am J Emerg Med. 1995 Sep;13(5):612-3. No abstract available.
PMID: 7662071 [PubMed – indexed for MEDLINE]

[3] 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]

[4] Randomised trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema.
Cotter G, Metzkor E, Kaluski E, Faigenberg Z, Miller R, Simovitz A, Shaham O, Marghitay D, Koren M, Blatt A, Moshkovitz Y, Zaidenstein R, Golik A.
Lancet. 1998 Feb 7;351(9100):389-93.
PMID: 9482291 [PubMed – indexed for MEDLINE]

[5] High-dose intravenous isosorbide-dinitrate is safer and better than Bi-PAP ventilation combined with conventional treatment for severe pulmonary edema.
Sharon A, Shpirer I, Kaluski E, Moshkovitz Y, Milovanov O, Polak R, Blatt A, Simovitz A, Shaham O, Faigenberg Z, Metzger M, Stav D, Yogev R, Golik A, Krakover R, Vered Z, Cotter G.
J Am Coll Cardiol. 2000 Sep;36(3):832-7.
PMID: 10987607 [PubMed – indexed for MEDLINE]

Free Full Text and Free PDF Download from ScienceDirect

[6] Administering a glyceryl trinitrate infusion: big is not always best.
Reed MJ.
Emerg Med J. 2007 Jun;24(6):423-4.
PMID: 17513541 [PubMed – indexed for MEDLINE]

Free Full Text from PubMed Central

[7] Administering a glyceryl trinitrate infusion: faster is better than slower.
Steel A, Varley J.
Emerg Med J. 2008 Jan;25(1):60. No abstract available.
PMID: 18156558 [PubMed – indexed for MEDLINE]

[8] Treatment of severe decompensated heart failure with high-dose intravenous nitroglycerin: a feasibility and outcome analysis.
Levy P, Compton S, Welch R, Delgado G, Jennett A, Penugonda N, Dunne R, Zalenski R.
Ann Emerg Med. 2007 Aug;50(2):144-52. Epub 2007 May 23.
PMID: 17509731 [PubMed – indexed for MEDLINE]

Free Full Text PDF Download from Ferne.org

[9] High dose nitroglycerin treatment in a patient with cardiac arrest: a case report.
Guglin M, Postler G.
J Med Case Reports. 2009 Aug 10;3:8782.
PMID: 19830240 [PubMed]

Free Full Text from PubMed Central

[10] 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

[11] 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

[12] Isosorbide dinitrate bolus for heart failure in elderly emergency patients: a retrospective study.
Freund Y, Delerme S, Boddaert J, Baker E, Riou B, Ray P.
Eur J Emerg Med. 2011 Oct;18(5):272-5.
PMID: 21499108 [PubMed – indexed for MEDLINE]

[13] Nitroglycerin for Treatment of Acute, Hypertensive Heart Failure: Bolus, Drip or Both?
Kwiatkowski GM, Saely S, Purakal J, Mahajan A, Levy PD/Detroit Receiving Hospital, Detroit, MI; Wayne State University School of Medicine, Detroit, MI
Annals of Emergency Medicine, Volume 60, issue 4 (October, 2012), p. S9.
ISSN: 0196-0644 DOI: 10.1016/j.annemergmed.2012.06.049
Abstract 22 Indexed with OhioLINK Journal Article Locator

[14] What is the basis for post-resuscitation treatment recommendations?
Rogue Medic
Mon, 15 Oct 2012

Kwiatkowski, G.M.; Saely, S.; Purakal, J.; Mahajan, A.; Levy, P.D. (2012). Nitroglycerin for Treatment of Acute, Hypertensive Heart Failure – Bolus, Drip or Both? Annals of Emergency Medicine, 60 (4), 59-59


What is the basis for post-resuscitation treatment recommendations?

We spend a lot of time worrying about how to get a pulse back. We spend so much time on getting that pulse back, that some of us think that producing a pulse is what matters.

Once we have a pulse back, whether using only evidence-based treatments (continuous compressions and defibrillation) or after throwing in some of the witchcraft that does not belong in the guidelines (ventilations, intubation, epinephrine, vasopressin, norepinephrine, phenylephrine, amiodarone, lidocaine, magnesium), we have no good evidence to guide treatment.

There is no proven benefit or harm associated with administration of routine IV fluids or vasoactive drugs (pressor and inotropic agents) to patients experiencing myocardial dysfunction after ROSC.[1]


This clearly rules out having any treatments categorized as Class I or even as Class IIa, but the AHA (American Heart Association) does not follow its rules for evaluation evidence. In the paragraph following the quote above, the guidelines state –

Fluid administration as well as vasoactive (eg, norepinephrine), inotropic (eg, dobutamine), and inodilator (eg, milrinone) agents should be titrated as needed to optimize blood pressure, cardiac output, and systemic perfusion (Class I, LOE B).[1]


Where is the evidence?

There is a paucity of data about which vasoactive drug to select first, although providers should become familiar with the differing adverse effects associated with these drugs, which might make a particular agent more or less appropriate for a specific patient.153 [1]


In other words, we should not select drugs because they are good, but because they do not have a lot of evidence of harm, or because we are comfortable with the excuses for the harm these drugs cause.

When presented with this kind of advice, we should always ask, What evidence do we have that any of these harmful treatments provide more benefit than harm?

In EMS, dopamine seems to be the drug of choice for shock (inadequate tissue perfusion, usually with hypotension).

Although low-dose dopamine infusion has frequently been recommended to maintain renal blood flow or improve renal function, more recent data have failed to show a beneficial effect from such therapy161,162 [2]

Are we asking the right questions?

Is vasoconstriction the solution to shock?

Is vasodilation the problem?

High doses of NTG were used in 22 patients, including 14 patients with acute MI and eight patients with advanced HF. All patients had critically low BP measured by cuff, and 18 had an unmeasurable BP and pulse.[3]


The doses shown are considered to be huge – even for patients who have very high blood pressures.

These patients do not have any blood pressure, or they have such very low blood pressure that it cannot be measured. The treatment is NTG (NiTroGlycerin or GTN – GlycerylTriNitrate in Commonwealth countries).

Almost any ACLS (Advanced Cardiac Life Support) instructor will tell you exactly what the result will be – death and course failure for refusal to accept the dogma of hypotension plus NTG = death.

I underlined all of the patients who received 25 mg NTG or more. A standard NTG tab is 0.4 mg. All of the underlined patients received an amount of IV (IntraVenous) NTG that is more than 60 times higher than the standard NTG dose.

In all of these patients, the blood pressure was too low to be obtained.

Click on the image to make it larger.


Almost all of the massive dose NTG patients survived.

If we are to believe the hypothesis that vasopressors are necessary to treat shock, improvement after NTG does not make sense.

If we are to believe the hypothesis that vasopressors are necessary to treat shock, improvement after huge NTG does is not possible.

Maybe we need to reconsider our beliefs.

We have developed a bias that is unduly influencing our treatment of our least stable patients.

We have developed a bias that is unduly influencing our treatment of our most easily harmed patients.


[1] Vasopressors
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 9: Post–Cardiac Arrest Care
Vasoactive Drugs for Use in Post–Cardiac Arrest Patients
Free Full Text from Circulation

[2] Table 2. Common Vasoactive Drugs
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 9: Post–Cardiac Arrest Care
Vasoactive Drugs for Use in Post–Cardiac Arrest Patients
Free Full Text from Circulation

[3] High dose nitroglycerin treatment in a patient with cardiac arrest: a case report.
Guglin M, Postler G.
J Med Case Reports. 2009 Aug 10;3:8782.
PMID: 19830240 [PubMed – in process]

Free Full Text from PubMed Central . . . . . Free Full Text PDF from PubMed Central