Rule #1 Is there extreme axis deviation during WCT
Rule #2 Is lead V6 all (or almost all) negative?
Rule #3 Is the QRS during WCT “ugly”?
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:
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.
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.
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.
08:27 More commorbidities and increasing age of OHOCA. Is Time for changing approach and terminology?
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:
Aggressive fluid resuscitation with cristalloids, and saline solutions in particular, can be detrimental in many ways:
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
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
World Health Organization relesead the 2014 guidelines for Community management of opioid overdose.
Here are some highlights from the guidelines of particular relevance for emergency medicine
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.
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.
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.
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.
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.
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.
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.
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.
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