You respond to a 72 y/o female complaining of shortness of breath. Upon arrival you find an average sized elderly female with tachypnea and pale, moist skin. She states that she can’t do anything without feeling very short of breath. This is the ECG you obtain on the patient, what are you thinking at this point?
Watch the video below for the full case review and interpretation.
You respond to a 65 y/o Male at his residence. His daughter, on scene, called 911 because she is worried about her father’s health. She states that he just hasn’t been acting right. “He is weaker than normal, and becomes short of breath very easily”. The patient himself is not thrilled about your presence. He is a rather obese man (about 400 lbs), and he is sitting in his recliner sans shirt or pants. His immediate area provides evidence that he doesn’t move
S – The patient states that he is always weak and it is normal for him to get short of breath when he gets up.
A – NKDA
M – Glucophage, Gabapentin, Albuterol, Singulair, Prevacid, Carevedilol, Enalapril, Digoxin, Aspirin, Oxygen
P – AMI, CHF, Asthma, Non-insulin dependent diabetes, AICD
L – Oreos and Orange Juice
E – Sitting in his chair
B/P: 61/37, Left Arm
SpO2: 83, on 2 lpm O2,
Pulse: 40 & regular
Resp: 30 & regular
Skin: Pale, cool, & clammy
You place your patient on the monitor and obtain the following 12-lead. What would you immediately ask your patient? What is your interpretation of the ECG? What treatments would you provide?
I’ve been at it again with the video tutorials. Here is a quick, two-part explanation of Bundle Branch Blocks. I explain what causes the ECG changes associated with bundle branch blocks to the best of my abilities within the short amount of time that Youtube allows.
Did you know that both types of bundle branch blocks require you to look at more than just lead V1 to truly identify them? If not, make sure you see part 2.
Intraosseous Versus Intravenous Vascular Access During Out-of- Hospital Cardiac Arrest – A Randomized Controlled Trial
For treatment of medical cardiac arrest patients, which is better – IO (IntraOsseous) or IV (IntraVenous) access for medication administration?
Since no medications have ever been demonstrated to improve survival from cardiac arrest (only chest compressions and defibrillation have), the most important consideration will be what method results in the least interruption of compressions and the least interference with defibrillation.
All patients eligible for inclusion in this study had their ﬁrst attempt at vascular access randomized to one of 3 locations: proximal tibial intraosseous, proximal humeral intraosseous, or peripheral intravenous. The proximal tibial insertion site was located medial to the tibial tuberosity, or just below the patella along the ﬂat aspect of the tibia. The proximal humerus insertion site was deﬁned as the greater tubercle of the anterior humeral head 1 cm proximal to the surgical neck of the humerus. Peripheral intravenous catheter placement could occur at any accessible peripheral vein but preferably at the antecubital fossa; the external jugular vein was not an option provided for catheterization.
Proximal humeral access point.
Does this hurt? No. The patients are unresponsive and pulseless (dead), but even live patients and EMS personnel (who have tried this on themselves) report very little pain.
Overall success took into account a failure to maintain initial vascular access during the course of resuscitation, which included needle dislodgement or the inability to successfully administer medications or ﬂuid at any time during the resuscitation.
Those would interfere with the one claimed benefit – ability to deliver medication.
There was no difference in time to success for either of the intraosseous routes compared with the peripheral intravenous route.
The time to success is interesting. The times for the humeral site are similar to the tibial IO and the IV for placement and first drug administration – at least at the low end of the IQRs (InterQuartile Ranges). The problem is that the upper end of the IQRs is much longer than for the other methods. This is in part due to the low number of patients, which is partially explained by the 13 protocol violations – all in favor of the tibial IO site. The lack of familiarity of paramedics probably also contributes, resulting in much longer times for some of the paramedics.
Finally, there were 13 protocol violations that favored the tibial intraosseous route, which may have been an indicator of bias among paramedics for that route and therefore could have resulted in confounding of the study results.
It may be that this group of paramedics was much more comfortable with the tibial IO, than with the humeral IO and this led to a greater likelihood of coming up with excuses for protocol violations. This may also have led to the performance differences. I have seen similar differences with the introduction of a new type of IV catheter to some services. There can be a lot of conscious and unconscious resistance to the new method, but after some familiarity develops, things tend to return to normal.
In the literature, intraosseous needle insertions have been linked to local wound infections, osteomyelitis, fat emboli, and compartment syndrome.18-20 During this study, there was no mechanism in place for EMS or hospital personnel to report complications in the use of the intraosseous device.
That would be good to know, but this was not one of the goals of the study.
The average weight of patients in the humeral intraosseous group was greater than that of individuals in either of the other 2 arms of the study. This increased weight may have been associated with a difﬁculty in obtaining or maintaining vascular access.
Weight can be a problem for any method of IV/IO access, so this is a very important limitation.
Weight – mean (SD)
Overall – 97.3 kg (2.7)
Humeral IO – 103.9 kg (6.5)
IV – 97.7 kg (3.8)
Tibial IO – 91.5 kg (3.9)
An average weight of 228.6 pounds (103.9 kg) in the humeral IO group, but only 201.3 pounds (91.5 kg) in the tibial IO group? 27.3 pounds difference (13.8% difference).
That strongly suggests a problem.
The proximal humerus can also prove tenuous during cardiac arrest because it is centered near the upper torso, where resuscitation efforts are occurring, including airway management, ongoing chest compressions, and rescuer interchange. The constant activity creates a tremendous amount of movement and further increases the risk of unintentional needle dislodgement, which was veriﬁed during the debrieﬁng session after each out-of-hospital cardiac arrest, with paramedics frequently citing entanglement of the humeral intraosseous line, leading to dislodgement.
The peripheral intravenous site is the most commonly used vascular access by all health care providers, yet it proved successful in less than 50% of cases in this study.
No matter how bad the success of the humeral IO was, the IV success was even worse – less than 50% first attempt success.
Do IOs improve outcomes?
IOs may make it less likely that compressions will be interrupted, but we cannot tell from this study.
IOs may make it more likely that potentially harmful medications will be given.
The most interesting numbers I saw were the total fluid infused – twice as much in the IV group as in either IO group. No explanation is given, other than the possible slower flow rate for an IO. This may help to prevent fluid overload for those patients not in need of having an IV line accidentally left wide open.
There is no evidence that IOs, IVs, tubes, or medications improve survival to discharge with a working brain.
ACLS drug therapy during CPR is often associated with increased rates of ROSC and hospital admission but not increased rates of long-term survival with good neurologic outcome.
Will this make the Three Stooges Pit Crew concept less of a comedy of errors to implement?
Probably not, but we can hope that the AHA does the right thing and eliminates all of the treatments that don’t work – ventilation, intubation, IV access, IO access, epinephrine, amiodarone, lidocaine,
atropine – wait, they actually did remove atropine, so there is hope.
 Intraosseous Versus Intravenous Vascular Access During Out-of-Hospital Cardiac Arrest: A Randomized Controlled Trial.
Reades R, Studnek JR, Vandeventer S, Garrett J.
Ann Emerg Med. 2011 Dec;58(6):509-16.
PMID: 21856044 [PubMed - in process]
 Medications for Arrest Rhythms
Part 8: Adult Advanced Cardiovascular Life Support
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 8.2: Management of Cardiac Arrest
Free Full Text Article with links to Free Full Text PDF download
Even though epinephrine (adrenaline) is used automatically in cardiac arrest, and there is evidence that epinephrine helps to produce a pulse (ROSC – Return Of Spontaneous Circulation), there is no evidence that epinephrine improves the only survival statistic that matters – discharge from the hospital with a brain that still works. There were so many deviations from assignment protocol in their 2009 study, that the authors decided to examine the results based on what treatment patients actually received. They refer to epinephrine as adrenaline, which is the same drug. I will use adrenaline for consistency.
Our randomized study was analyzed on an intention-to-treat basis.4 As expected; some patients in the intravenous group had achieved ROSC before adrenaline could be given, while some in the no-intravenous group received adrenaline for different reasons. For example, it was permitted to place the IV line 5 min after ROSC. If re-arrest occurred, adrenaline could be administered if indicated by the CPR guidelines.7 
In the no andrenaline group, 37 of the 433 patients did receive andrenaline.
In the adrenaline group, 85 of the 418 patients did not receive andrenaline.
For 3 patients, the authors were unable to tell whether andrenaline was given and these patients were excluded.
This changes the data to 367 patients in the adrenaline group and 481 patients in the no adrenaline group.
Patients in the adrenaline group were more likely to be admitted to hospital and an intensive care unit compared to the no-adrenaline group (OR 2.5 CI 1.9, 3.4 and OR 1.4 CI 1.0, 1.9, respectively). 
This is nothing new. Patients receiving andrenaline are more likely to have ROSC. All that really matters is what happens after ROSC.
If the patient loses pulses after ROSC, giving more adrenaline may not produce the desired effect – another ROSC.
First look at Table 1. The duration of CPR is much longer with the adrenaline group. Is this because of patients losing pulses?
You can also see how few drugs were given to the no adrenaline group. They were not supposed to receive any drugs, but the use of adrenaline was the only criterion for reassigning patients in this reanalysis of the data. Atropine was given to 2% of the no adrenaline group and amiodarone was given to 2%. Was there overlap of these patients? We can’t tell.
The defibrillations were also significantly different. More patients were shocked in the adrenaline group, but more patients in the adrenaline group were in VF (Ventricular Fibrillation) initially. How many of the patients with PEA (Pulseless Electrical Activity) or Asystole developed VF after adrenaline? More shocks were also used for each patient. Was this due to rearrest?
Now looking at Table 2
Adrenaline starts out 2 1/2 times more likely to produce a pulse (ROSC), but a lot of those patients appear to have lost those pulses before admission to the hospital, since Table 2 shows that 69 of the 175 adrenaline patients admitted with CPR (CardioPulmonary Circulation) in progress. Adrenaline wears off in several minutes and produces a lot of undesirable side effects.
More is not better, especially since the doses of adrenaline being given are already many times larger than would be given to any living human.
Most important is the neurological function. I do not want to be resuscitated with only enough neurological function to spend the rest of my life watching reality TV in a long term care facility, or worse. That is not a successful resuscitation.
Adrenaline = 48% admitted to the hospital, but only 6% alive one year later.
No adrenaline = 27% admitted to the hospital, but 12% alive one year later.
Adrenaline (epinephrine) is not just changing the location of death, but is cutting overall survival in half.
Is getting pulses back a good enough reason to kill half of the patients who could survive?
Of the patients admitted to the hospital, 11% of the adrenaline group were discharged with good brain function.
Of the patients admitted to the hospital, 45% of the no adrenaline group were discharged with good brain function.
Of the patients admitted to the hospital, 12% of the adrenaline group were alive one year later.
Of the patients admitted to the hospital, 44% of the no adrenaline group were alive one year later.
The actual use of adrenaline may be a surrogate marker for patients with bad prognosis, but that has previously only been published from studies without a group randomized to not receiving drugs.21 
There are many limitations of this study, but the authors do not pretend that this is the final answer on adrenaline (epinephrine) in cardiac arrest. They do point out that we are not providing good care by continuing to use adrenaline without studying the outcome that matters – survival with good neurological function.
5% of the no adrenaline group survivors had significant brain damage.
20% of the adrenaline group survivors had significant brain damage.
Maybe the good news is that adrenaline does not produce a lot of survivors.
See also -
 Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial.
Olasveengen TM, Sunde K, Brunborg C, Thowsen J, Steen PA, Wik L.
JAMA. 2009 Nov 25;302(20):2222-9.
PMID: 19934423 [PubMed - indexed for MEDLINE]
 Outcome when adrenaline (epinephrine) was actually given vs. not given – post hoc analysis of a randomized clinical trial.
Olasveengen TM, Wik L, Sunde K, Steen PA.
Resuscitation. 2011 Nov 22. [Epub ahead of print]
PMID: 22115931 [PubMed - as supplied by publisher]
I am continuing to look for evidence that droperidol deserves to be given a
scarlet letter black box warning. The authors of this literature review take a look at several articles and some case studies.
Because the outcome of interest, sudden death caused by torsades de pointes, is uncommon and difficult to assess, QT prolongation has become a surrogate marker for potential arrhythmogenicity and is therefore commonly used in research and by regulatory agencies.18
Surrogate endpoints are great for making it seem that we know more than we actually do know. When there is not enough information, surrogate end points are a way of saying, If this belief is true, and this other belief is also true, then Treatment Z is safe (or dangerous), or saves X number of lives per year (or kills X number of patients who otherwise would have been expected to live).
The example that I repeatedly use is the Cardiac Arrhythmia Suppression Trial, which ended up demonstrating that treatment based on the surrogate endpoint of eliminating PVCs (Premature Ventricular Contractions) because they are associated with a higher rate of death actually resulted in tens of thousands of extra deaths. That is the difference between looking at surrogate endpoints (making assumptions about death rates) and looking at actual death rates.
a consistent relationship between the length of the QT interval and the risk of torsades de pointes or sudden death is not clearly established and might vary from drug to drug and from individual to individual. Hundreds of drugs are known to prolong the QT interval, with widely variable degrees of evidence for clinical dysrhythmias.16,17 
What did the authors find?
Because of the small number of studies and articles identified, we were unable to perform a true systematic review (ie, meta-analysis)22 
First, what does the FDA (Food and Drug Administration) label recommend as the dosage of droperidol?
Adult Dosage: The maximum recommended initial dose of droperidol is 2.5 mg I.M. or slow I.V. Additional 1.25 mg doses of droperidol may be administered to achieve the desired effect. However, additional doses should be administered with caution, and only if the potential benefit outweighs the potential risk.
As if that caution does not apply to the use of every medication.
In one surgical study of 40 patients receiving three weight-based doses of droperidaol, which if given to a 70 kg adult, would be doses of 7 mg, 12.25 mg, and 17.5 mg. Much higher than 2.5 mg. Yes, this is surgery, so what does the FDA recommend about surgical dosing?
Dosage should be individualized. Some of the factors to be considered in determining dose are age, body weight, physical status, underlying pathological condition, use of other drugs, the type of anesthesia to be used, and the surgical procedure involved.
They certainly were not excluding surgery from their dosing recommendation.
QTc interval prolongation occurred within 1 minute of injection and did not increase with time. Prolongation of the median QTc interval occurred by 37, 44, and 59 ms, respectively, in a dose-dependent fashion; this was also statistically significant (P<.003). 
Of these patients receiving very high doses, how many died?
No dysrhythmias developed. 
There was a lower dose surgical study and a long-term psychiatric study. Again, there was QT prolongation, but no arrhythmia (dysrhythmia and arrhythmia are synonyms).
And there is one ED (Emergency Department) retrospective study –
Over a 4-year period, 15,374 patients received 18,020 doses of droperidol. Of the 682 patients who had an ECG performed after droperidol administration, 14 (3.1%) had prolonged QT intervals (defined as >480 ms) without evidence of any bundle branch block. Four of the 14 patients had previously documented prolonged QT intervals not associated with droperidol use. A control group (n=100) who had ECGs performed without the administration of droperidol had a similar incidence of prolonged QT intervals (4.0%). 
The patients who received droperidol appear to have been less likely to develop QT segment prolongation. With droperidol – 3.1% had QT prolongation. Without droperidol – 4.0% had QT prolongation.
The control group only had 100 patients, so each patient represents 1.0%, but if droperidol is so dangerous there should be more QT prolongation in the droperidol group. Maybe there is something about the way that droperidol is used in the ED that decreases the supposed danger.
These studies do not mean that droperidol is safe, but they do raise questions about the rush to add a black box warning to the droperidol label.
With the black box warning, the FDA essentially says, Lawyers, look here. You don’t have to demonstrate that droperidol is dangerous – we did that for you. Go sue some doctors.
These studies do not support the claim by the FDA that droperidol is dangerous. In Part II, I will continue with the case studies reviewed by the authors.
 Droperidol, QT prolongation, and sudden death: what is the evidence?
Kao LW, Kirk MA, Evers SJ, Rosenfeld SH.
Ann Emerg Med. 2003 Apr;41(4):546-58. Review.
PMID: 12658255 [PubMed - indexed for MEDLINE]
 Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial.
Echt DS, Liebson PR, Mitchell LB, Peters RW, Obias-Manno D, Barker AH, Arensberg D, Baker A, Friedman L, Greene HL, et al.
N Engl J Med. 1991 Mar 21;324(12):781-8.
PMID: 1900101 [PubMed - indexed for MEDLINE]
CONCLUSIONS. There was an excess of deaths due to arrhythmia and deaths due to shock after acute recurrent myocardial infarction in patients treated with encainide or flecainide. Nonlethal events, however, were equally distributed between the active-drug and placebo groups. The mechanisms underlying the excess mortality during treatment with encainide or flecainide remain unknown.