The “3 SIMPLE Rules”: an easy and accurate tool for recognizing VT

17 dic
Following the discussion on ectopy and aberrancy (view Ectopy or aberrancy? Google Ecg+ community comments on a clinical case.)  Ken Grauer, EKG master and author of many EKG books, gave us the permission to share his “3 SIMPLE Rules” to recognize VT in a simple ad accurate way.
  • Rule #1 Is there extreme axis deviation during WCT

Extreme axis deviation is easy to recognize. The QRS complex will be entirely negative in either lead I or lead aVF. The presence of extreme axis deviation during a WCT rhythm is virtually diagnostic of VT.
  • Rule #2 Is lead V6 all (or almost all) negative?

IF ever the QRS in lead V6 is either all negative (or almost all negative)  then VT is highly likely.
  • Rule #3 Is the QRS during WCT “ugly”?

The “uglier” the QRS the more likely the rhythm is. VT originates from a ventricular focus outside of the conduction system. As a result VT is more likely to be wider and far less organized (therefore “uglier”) in its conduction pattern
The “3 simple rules” is an extract from ACLS 2013 Arrhythmias  where you can find the complete explanation and much more on arrhythmias.
Visit Ken Grauer Amazon page to find out more and discover all the amzing EKG books he wrote. They are accurate and reliable for use in many emergency situation.
I’ll include Ken’s reply in the main script of the post cause it contains some very important adjuncts and expalnations. At the end of the replay you’ll find the link to download the full text of the section regarding the WCT topic. You’ll also appreciate the perfect Ken’s italian. I’m amazed….
Molto grazie Mario per la pubblicazione del mio consiglio su le tre semplici regole per diagnosticare VT! I’ll make a few brief additions to what Mario wrote. RULE #1 – Remember that slight or even moderate axis deviation is of no help. The QRS complex must be ALL negative in either lead I or in lead aVF. If it is – then the rhythm is almost always VT. RULE #2 – Again, moderate negativity in lead V6 is common and means nothing. But if the QRS complex in lead V6 is either all negative or shows no more than a tiny r wave – then VT is likely. This is because such marked negativity in lead V6 implies that the impulse is moving away from the apex – and that almost always means VT. RULE #3 – Supraventricular rhythms with either preexisting bundle branch block or aberrant conduction typically resemble some form of conduction defect (ie, either RBBB, LBBB or RBBB with LAHB and/or LPHB). However, if the QRS complex is amorphous (ie, very “ugly” and formless) – then it is much more likely to be originating from the ventricles. Occasionally, patients may have unusual forms of IVCD – so this rule is not 100% accurate – but it is a helpful supportive point in the differential diagnosis. For those wanting more complete description of the 3 Rules (and other pointers in assessing wide tachycardias) – feel free to download these Sections from my ACLS-2013-ePub – GO TO – – Detailed description of the 3 Simple Rules begins in Section 08.17. Spero che questo vi aiuta.”
Ken Grauer

Ectopy or aberrancy? Google Ecg+ community comments on a clinical case.

16 dic
 75 yrs old female, confused, chest pain and hypotensive. Below ypu can see the 12 leads EKG pre and post cardioversion


EK post cardio

The question about ectopy and aberrancy, even if of minor influence on theraphy that was based on clinical presentation, was interestingly debated in ECG+ community.

Prof. Ken Grauer and other members of community gave the solution on why the above 12 leads EKG was, with good approximation, referrable to a VT and not to a SVT conducted with aberrancy.

Those are the EKG criteria they individuated:

  1. Extreme axis “northwest axis”: (neg in lead I, positive in lead aVR);
  2. Lead V1 is amorphous
  3. Lead V6 is almost all negative
  4. No diphasic RS complexes in any of the precordial leads
  5. Monophasic R-wave in lead V1(taller left “rabbit-ear”)
  6. Diphasic QR complexes in leads V2 and V3.
  7. Monophasic QS complexes in leads V4, V5, and V6.
  8. Josephson’s sign (notching on the nadir of S wave)

Those criteria, even if present in this case, are universally valid.

If you want to discover more on this topic MEDEST already posted on this topic in a previous post

There you can find alle the references on EKG criteria for differential diagnosis between ectopy and aberrancy in wide comples tachycardia.




M(orphine)O(xygen)N(itrates)A(SA) in STEMI. New evidences indicates that is time to change our practice

26 nov

In a previous post we already told about a possible interaction between Morfine and antiplatelets therapy, proposing, on the base of the new evidences, a different approach to analgesia in AMI with a more caution morphine administration in STEMI patients.

Courtesely from Dott. Guido Parodi

Courtesely from Dott. Guido Parodi

A recent published study, presented at American Heart Association (AHA) 2014 Scientific Sessions, also questioned oxygen use in non hypoxic STEMI patients.

The Air Versus Oxygen in ST-Elevation Myocardial Infarction (AVOID) trial compared supplemental oxygen vs no oxygen unless O2 fell below 94%.

“The AVOID study found that in patients with ST-elevation myocardial infarction who were not hypoxic, there was this suggestion that, potentially, oxygen is increasing myocardial injury, recurrent myocardial infarction, and major cardiac arrhythmia and may be associated with greater infarct size at 6 months,” lead author Dr Dion Stub (St Paul’s Hospital, Vancouver, BC, and the Baker IDI Heart and Diabetes Institute, Melbourne, Australia) concluded.

A previous Cochrane review Oxygen therapy for acute myocardial infarction. Cochrane Database Syst Rev 2013 concluded that “current evidence neither supports nor clearly refutes the routine use of oxygen in people with AMI”, so after AVOID trial the ideal balance is more and more weighing on avoiding supplemental oxygen in STEMI non hypoxic patients.

We can affirm now that 50% of MONA acronym is, at least, reasonably questionable, and a new era in the treatment of STEMI patients is probably coming.



A great Twitter day!

24 nov
TwitterI’m more and more convinced of the power of spreading informations and resources trough social media.
Twitter is something that you can’t miss if you want to stay on the line of medical education. Conferences, articles, discussions and much more flows on twitter line everyday.
So give a look at MEDEST timeline of today and read text articles treating different aspects of emergency medicine.

24’th November, 2014 @medest118

08:10 Improved Survival After Out-of-Hospital Cardiac Arrest and Use of Automated External Defibrillators

08:15 Treatment for Out-of-Hospital Cardiac Arrest Is the Glass Half Empty or Half Full?t

08:27 More commorbidities and increasing age of OHOCA. Is Time for changing approach and terminology?

08:33 It is time to embrace an era in which transparency and responsible data sharing are common values. 

08:35 Glucocorticoids as an Emerging Pharmacologic Agent for Cardiopulmonary Resuscitation

08:42 Sedation in non-invasive ventilation: do we know what to do (and why)?

08:50 Diagnosis and acute management of anaphylaxis

08:54 Are you ready for running Florence marathon on 30 Nov?

14:38 Il ventilatore polmonare vi spaventa? avete sempre desiderato utilizzarlo ma non avete mai osato?

If you don’t already have one, get a Twitter profile and

Follow MEDEST on Twitter @medest118

You can also follo us on Facebook


Acute Pulmonary Edema: Myths and Facts

16 nov
A Storify report by: Anand Swaminathan @EMSwami  from


  • Preamble:

Minimal change in therapeutic approach to APE over 40 years despite modern evidences.

In APE (Acute Pulmonary Edema), the first ten minutes of management dictate the course of the patient. This is where we can save a life.


  • Pathophysiology

Cardiorenal model basis for use of furosemide is mechanistically flawed and outdated.

Cardiocirculatory model: peripheral vasoconstriction leads to decrease in  cardiac function.

Neurohormonal model: build on increased norepinephrine levels and renin-angiotensin-aldosterone system activation


Urban Legend #1 – Loop diuretics are 1st line therapy in treatment of APE

The Truth #1 – Loop diuretics are not recommended as 1st line treatment in APE


Urban Legend #2 – Patients presenting with APE are volume overloaded

The Truth #2 – Most patients with APE are not fluid overloaded and thus, do not require diuresis. Vascular Congestions DOES NOT equal fluid overload

  •  most pt w/ APE have incr cardiac filling pressure but minimal change in baseline/dry weight
  •  > 50% pt w/ APE had weight gain < 2 lbs on presentation
  •  Pulm edema results from fluid shifts not fluid gain


Urban Legend #3 – Loop diuretics are harmless in APE treatment so just give them

The Truth #3 – Loop diuretics are harmful early in the management of APE and should be withheld



Urban Legend #4- Morphine should be part of the initial APE algorithm

The Truth #4- Morphine is harmful in APE and should be completely dropped from treatment algorithm



Bottom line:


  • Loop diuretics are 1st line therapy in treatment of APE

  • Patients presenting with APE are volume overloaded

  • Loop diuretics are harmless in APE treatment so just give them

  • Morphine should be part of the initial APE algorithm


  • Loop diuretics are not recommended as 1st line treatment in APE

  • Most patients with APE are not fluid overloaded and thus, do not require diuresis

  • Loop diuretics are harmful in early phases of the management of APE and should be withheld

  • There is no role for furosemide in the management of APE

  • Morphine is harmful in APE and should be completely dropped from treatment algorithm

Fluid resuscitation in bleeding trauma patient: are you aware of wich is the right fluid and the right strategy?

8 nov

DCR copy

The fluids of choice in prehospital field are, in most cases, cristalloids (Norma Saline or Lactate Ringer).

But what is the physiological impact of saline solutions when administered in large amounts (as the latest ATLS guidelines indicates) to hypotensive trauma patients?

Is aggressive Fluid resuscitation the right strategy to be pursued?

The triad of post-trauma lethal evolution is:

  • Hypotermia
  • Acidosis
  • Coagulopathy

Aggressive fluid resuscitation with cristalloids, and saline solutions in particular, can be detrimental in many ways:

  1. Cristalloids tend to displace the already formed clots and improves bleeding
  2. Normal Saline produce hypercloremic acidosis worsening coagulation and precipitating renal and immune dysfunction
  3. Cristalloids diluts the coagulation factors and precipitate the coagulation system (dilution coagulopathy)
  4. Cristalloids rapidilly shift in intercellular space worsening SIRS process and interstitial edema (brain edema, bowel wall edema) with consequent compartment hypertension

So wich is the perfect fluid to infuse in trauma?

The perfect fluid doesn’t exists.

Balanced saline and Hypertonic saline are promisng prospective but there are still no good quality evidences about their benefit on clinical outcomes.

Colloids has no place in fluid resuscitation of trauma patients.

The fluid of choice, regarding the actual evidences and indications, is Lactate Ringer.

More than on the type of fluid the attention of researchers and clinicians is oriented on the strategy to pusue in those cases.

Hypotensive resuscitation, part of damage control resuscitation, is at the moment the strategy of choice in trauma bleeding patients.

Restrictive fluids administration is the way to achieve this goal.

The target systolic BP has to be diferentiated depending on the type of trauma

  • 60–70 mmHg for penetrating trauma
  • 80–90 mmHg for blunt trauma without TBI
  • 100–110 mmHg for blunt trauma with TBI.

More important do not delay definitive treatment.

ASAP give blood products (PRBC, FFP etc…) to contrast post-trauma coagulopathy and send the patients in OR to fix treatable causes of bleeding

The following are a collection of  un essentials resources on haemostatic resuscitation after trauma



Community management of opioid overdose

6 nov

World Health Organization relesead the 2014 guidelines for Community management of opioid overdose.

Reccomendation 1

Here are some highlights from the guidelines of particular relevance for emergency medicine

  • Formulation and dose of naloxone

Route of administration
The GDG recognizes that the IV route is appropriate and effective in medical settings
The capacity of the nasal mucosa to absorb liquids is limited, so if the intranasal route of administration is to be used, concentrated forms of naloxone should ideally be used.
The GDG has made this recommendation fully aware that the intranasal route is currently an off-label (non-licensed) route.
Affordability may dictate the preferred route in particular contexts
The choice of initial dose will depend on the formulation of naloxone to be used and the context.
In medical settings dose selection is not generally an issue as dose titration is standard practice. In non-medical settings dose titration is not so easily accomplished and higher initial doses may be desirable.
The context also dictates the total amount of naloxone made available to non-medical responders.
The initial dose should be 0.4mg–2mg, targeting recovery of breathing. In most cases 0.4–0.8 mg is an effective dose. It is important to provide sufficient naloxone to supplement the initial dose, as necessary.

Intranasal delivery may require a higher dose. It should be noted that the commonly used method of intranasal administration is to spray 1 ml of the 1 mg/ml formulation of naloxone into each nostril with an atomizerconnected to a syringe.

Where possible, efforts should be made to tailor the dose to avoid marked opioid withdrawal symptoms. The GDG notes that higher initial doses above 0.8 mg IM/IV/SC are more likely to precipitate significant withdrawal symptoms.

A more complicated situation arises where there has been an overdose of a combination of drugs. In this situation naloxone is still beneficial for reversing the opioid intoxication component of the overdose.


  • Cardiopulmonary resuscitation

In suspected opioid overdose, first responders should focus on airway management, assisting ventilation and
administering naloxone.
Because the key feature of opioid overdose is respiratory arrest, ventilation is a priority. While recognizing there are different protocols in different parts of the world, the GDG suggests the following steps in resuscitating an individual with suspected opioid overdose.
Apply vigorous stimulation, check and clear airway, and check respiration – look for chest rising and falling.
In the presence of vomit, seizures or irregular breathing, turn the patient on their side, and, if necessary, clear the airway of vomit.
In the absence of regular breathing provide rescue ventilation and administer naloxone.
If there are no signs of life, commence chest compressions.
Re-administer naloxone after two to three minutes if necessary
In all cases call for professional assistance.
Monitor the person until professional help arrives.
  • Post resuscitative care

After successful resuscitation following the administration of naloxone, the affected person should have their level of consciousness and breathing closely observed until they have fully recovered.
The definition of ‘fully recovered’ is a return to pre-overdose levels of consciousness two hours after the last dose of naloxone.
Ideally, observation should be performed by properly-trained professionals.
The period of observation needed to ensure full recovery is at least two hours, following overdose from short-acting opioids such as heroin. It may be longer where a longer acting opioid has been consumed.
If a person relapses into opioid overdose, further naloxone administration may be required.
The definition of ‘fully recovered’ is a return to pre-overdose levels of consciousness two hours after the last dose of naloxone

Download the full guidelines at



Bougie aided video assisted intubation through King Laryngeal Tube

31 ott

If you have a patient with a King LT in place and want to intubate him use the Bougie and the videolaryngoscope. It works perfectly.

Here is the video tutorial.


How a perfect ALS can kill: Pulseles Electric Activity a novel approach in medical cardiac arrest.

27 ott

HOW PERFECT ALS CAN KILLHEMS arrives on a patients where ground medical service is conducting a perfect ALS.

The 50 years old pt is in PEA cardiac arrest (CA) (sinus bradycardia narrow QRS) airway secured with an 8 ET. The pt was still pulseless (double checked) after almost 20 min of CA, 6 mg of epi already administered and good quality chest compression was ongoing. EtCO2 was 35 (!!!!) even when chest compression were stopped for the pulse check(!!!).

Still no palpable pulse. At this point a 12 lead EKG was performed (against alla the ALS dogmas) with the patient still pulseless and the chest compressions were conseguently suspended (other ALS eresia) while placing the precordial leads and acquiring the EKG.

EKG result: Sinus Rithm 50 bpm. Inf+dx STEMI with reciprocal changes in lateral leads.

S…t she is alive!!! This is not PEA but profound cardiogenic shock.


Pulseles Electric Activity a novel approach in medical cardiac arrest

When classical ALS algorithm comes to non defib rithm says that asystole and PEA are the same and have to be equally treated.

There is not such a clinical and therapeutic mistake.

Cardiac stand still and contractile cardiac activity without a palpable central pulse are totally different issues.Pulseless electric activity in the majority of cases is more like a profound state of shock than an asystole, and like this has to be treated.

But let’s make just a step backword.

First cosideration is on the identification of pulseless patients.

At the moment official guidelines consider a pulseless patient based on the palpation of carotid pulse. ERC BLS 2010 official guidelines about carotid pulse palpation says: “Checking the carotid pulse (or any other pulse) is an inaccurate method of confirming the presence or absence of circulation, both for lay rescuers and for professionals” so is no long recommended.

So why if is no recommended for BLS is used in ALS guidelines to recognize pulseless patients and to treat them as an asystolic one? Is our finger a reliable instrument to decide beetwen life and death? Even the BLS guidelines give us the answer: NO.

Second consideration is the research of the underlyng causes of PEA.

The H’s and T’s classification is an etiologic definition and not a clinical one and is often impossible to use in emergency settings cause of the lack of clinicla informations.

Norman and Desbiensin their 2008 article Simplifying the diagnosis and management of pulseless electrical activity in adults: A qualitative review proposed a new classification based on a more clinical concept that is somehow useful for the emergency clinicians.

3 and 3 rule, even if still not validate, seems more helpful for clinicians working on the field or at least for quick use in emergency situation. On plus give us a guide for tretment according on patophisiologic origin of PEA.

3+3+3 rule



More recently Littmann, Bustin and Haley in the 2013 article “A Simplified and Structured Teaching Tool for the Evaluation and Management of Pulseless Electrical Activity” use EKG findings to guide the diagnosys of cause of PEA and to treat it. On the base of QRS duration they identify a possible origin, mechanical or metabolic, and accordingly propose the specific treatment.

PEA evaluation algo









PEA evaluation algo1PEA evaluation algo2


















The introduction of point of care echo and EtCO2 in ED and on the field put a new brick in definition, diagnosys and treatment of PEA.

Ultrasonography give us the chance to expolore, confirming or excluding, most of the mechanical causes of PEA and EtCO2 is a more reliable indicator of perfusion than the subjective pulse palpation.

Regarding the tretment options, there are still no evidences in favour or against epinephrine administation and chest compression utility in patients pulseless with electric activity and no cardiac standstill.

The end of clinical case

After performing 12 leads EKG the patients was loaded on the helicopter and directed to the cat lab where the patients arrived still pulseless but with EtCO2 38. The angio, performed after an echo showing weak heart contractility with inferior wall ipokinesia, confirmed critical occlusion of the dx coronary artery. A medicated STENT was placed with good TIMI flow result.

The patient regained consciouness a couple of hours later, and was dismissed from the hospital afer 15 days with CPC 1 and 45% EF.

In this case the strict observance of ALS protocol would have conducted the medical team to continue CPR, despite the presence of a organized rythm, due to the absence of a palpable central pulse. Epinephrine would have been regularry administered (at CA doses) and chest compressions performed.

The decision to load and go to the PCI center gave the patient the chance to treat the underlyng cause of CA.

Not the same thing can be said about the ALS protocol.







Progressi nel soccorso extraospedaliero: utilizzo del VAR in emergenza urgenza extraospedaliera

24 ott

On line le slide della mia presentazione al congresso nazionale SIS 118 2014 in svolgimento a Santa Margherita Ligure




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