Introducing Open, Post-Publication, Expert Peer Review on ALiEM

ExpertPeerReviewStamp2x200Today, we are busting open the concept of peer review for publications on blogs!

The peer review process has been criticized for its flaws, but is universally accepted as a necessary part of the scientific process. Peer reviewing allows experts in a field to determine the validity of a study or an article so that those of us who are less expert can reap the benefits of their knowledge. Until recently this process was almost universally pre-publication and anonymous.  Authors would go through months of review and revision based on feedback of experts whose name they didn’t even know. In the last decade journals such as BMJ Open moved to an open peer review process by divulging the reviewer’s identities to the author and publishing the reviews of the experts online for open access to all readers. This open peer review model prevents redundancy and encourages transparency in the scientific process.

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Bundle Branch Blocks (BBBs) 101

722px-Electrical_conduction_system_of_the_heartRecently, I have been asked by several students at my home institution (UTHSC at San Antonio) to help them understand bundle branch blocks.  This is different than some of my usual posts because it is meant to be more educational than evidence based.  So here we go.  The normal conduction system of the healthy heart is shown to the right.  If there is a delay or block in the left or right bundle, depolarization will take longer to occur. Therefore we get a widened QRS (>0.12 sec or >3 small boxes).

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PV Card: Brugada Criteria for SVT with Aberrancy vs Ventricular Tachycardia

2011_04_22Awm

Due to the overwhelming popularity of Dr. Salim Rezaie‘s recent post discussing the Brugada criteria for  SVT with aberrancy vs VT, Dr. Jason West (@JWestEM, an EM resident from Jacobi/Montefiore) kindly helped to co-author and package this information into a PV card for quick reference. To use this sequential, four-question approach, if at any time you answer YES to the question, it is ventricular tachycardia.

PV Card: SVT vs VT – Brugada Criteria


Adapted from [1]
Go to ALiEM (PV) Cards for more resources.

Reference

  1. Brugada P, Brugada J, Mont L, Smeets J, Andries E. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation. 1991;83(5):1649-1659. [PubMed]

Choosing the right vasopressor agent in hypotension

Hypotension vasopressor selection

The incidence of critical illness in the ED is rising, with greater than 1 million ED patients requiring emergent resuscitation each year. In addition to definitive airway management, hemodynamic support is among the most important life-saving interventions implemented by emergency physicians. When a patient develops persistent hypotension, what is your approach to choosing the right vasopressor medication for hemodynamic support?

Persistent hypotension results in impaired tissue perfusion and is often a late and ominous indication of decompensated shock. Correction of persistent hypotension is imperative, often requiring vasopressors and inotropes. When considering an agent for hemodynamic support, the following checklist can guide your choice: 1–4 

1. Why is the patient hypotensive?

Identifying the cause of the hypotension will allow you to select an agent targeted to the source of the problem. Causes of hypotension include hypovolemia, impaired vascular tone, impaired pump function, or some combination of these problems.

2. Have I optimized volume status and ruled out other diagnoses?

Initial management of the hypotensive patient should target optimizing intravascular volume prior to initiating a vasoactive medication. Vasopressors or inotropes cannot improve malperfusion secondary to isolated hypovolemia (such as hemorrhage, gastrointestinal bleeding or severe dehydration), and use of these agents prior to volume resuscitation can exacerbate existing metabolic derangements. Unrelated conditions that impair preload or cardiac output, including tension pneumothorax and pericardial tamponade, should also be considered prior to initiating vasoactive therapy.

3. How can I pharmacologically redirect blood flow to improve the problem?

Selecting an agent for hemodynamic support is analogous to choosing an antibiotic for infection. You are best guided by matching medication activity to the underlying pathology of the illness.

  • Problem with VASCULAR TONE? Phenylephrine is the only agent with exclusive activity at α adrenergic receptors, and vasopressin is the only agent with activity at vasopressin receptors. In this sense, these are pure pressor agents and have no direct impact of pump function. Hypotension from isolated loss of vascular tone is uncommon but can be caused by loss of sympathetic tone from spinal cord injury (“neurogenic shock”).
  • Problem with PUMP FUNCTION? Hypotension attributable to isolated acute myocardial compromise can be improved with pharmacologic agents that increase inotropy and contractility. This includes any agent with action at β1 , β2 or dopaminergic receptors. Dobutamine and isoproterenol are the only agents with exclusive activity at β adrenergic receptors. Generally, these are pure intropes and have no vasoconstrictive properties. Hypotension from isolated pump failure can be caused by acute decompensated heart failure or acute coronary syndrome.
  • MULTIFACTORIAL problem? Problems that impact both vascular tone and cardiac function require medications that operate at multiple receptors. These include epinephrine, norepinephrine and dopamine. The physiologic impact of dopamine is dose dependent, with preferential increases in pump function at lower doses. Examples of disorders that impact both pump and tone include anaphylaxis (see “Dirty Epi” drip) or septic shock.

4. Will I be limited by side effects of my pressor choice?

Side effects of vasoactive medications are related both to the direct mechanism of action of the agent, as well as the compensatory mechanisms precipitated by them. Concerning side effects of inotropes include dysrhythmias and increased myocardial oxygen demand, whereas vasopressors can cause undesired limitations in blood flow to the gut and kidneys.

 

AgentPrimary ReceptorPrimary ImpactPotential side effectPrototypical clinical scenario
Phenylephrineα1 Increased SVRReflexive decreased HRNeurogenic shock
VasopressinVIncreased SVRDecreased splanchnic flowAdjunct for septic shock
Dobutamineβ1, βIncreased inotropyTransient decreases in SVR (βagonsim)Cardiogenic shock from late-stage heart failure
Dopamine (low-dose)D, β1Increased inotropy and heart rateTachydysrhythmiasCardiogenic shock, particularly if bradycardic
Epinephrineα1, α2, β1, βIncreased SVR and inotropyTachydysrhythmias and decreased splanchnic flowAnaphylaxis
Norepinephrineα1, α2, β1>> β2*Increased SVR and inotropyDecreased splanchnic and renal flowSeptic shock
Dopamine (high-dose)D, α1, β1>> β2*Increased SVR and inotropyTachydysrhythmias and decreased splanchnic/renal flowBradycardic cardiovascular collapse
* Controversial whether norepinephrine and high-dose dopamine have any βeffects. If any, it is likely very low.

5. When choosing between similar agents, does evidence support use of a specific agent over another?

The majority of evidence comparing pressors head-to-head has been done in patients with septic shock; the largest amount of data has compared high-dose dopamine to norephinephrine. Based on this data, norepinephrine has been associated with lower incidence arrythmias and improved mortality when compared to dopamine.

Epinephrine has been compared with several other regimens both in septic shock and undifferentiated shock. When epinephrine was compared to norepinephrine and dobutamine, all of the agents were equally effective in achieving hemodynamic goals, though epinephrine was associated with increased incidence of tachydysrhythmias and prolonged metabolic derangement when compared to other agents. There was no difference in mortality. Robust data comparing other similar agents in other disease processes are lacking.

 

References

1.
Myburgh J, Higgins A, Jovanovska A, et al. A comparison of epinephrine and norepinephrine in critically ill patients. Intensive Care Med. 2008;34(12):2226-2234. [PubMed]
2.
Ellender T, Skinner J. The use of vasopressors and inotropes in the emergency medical treatment of shock. Emerg Med Clin North Am. 2008;26(3):759-86, ix. [PubMed]
3.
Vasu T, Cavallazzi R, Hirani A, Kaplan G, Leiby B, Marik P. Norepinephrine or dopamine for septic shock: systematic review of randomized clinical trials. J Intensive Care Med. 2012;27(3):172-178. [PubMed]
4.
De B, Aldecoa C, Njimi H, Vincent J. Dopamine versus norepinephrine in the treatment of septic shock: a meta-analysis*. Crit Care Med. 2012;40(3):725-730. [PubMed]

A time-based approach to elderly patients with altered mental status

clockIt’s 7 am on a Monday. Your first patient is an 82 year-old woman who was brought in by EMS from an assisted living facility. All EMS can tell you is that she was not acting herself. You enter her room and introduce yourself. “Hello Mrs. Jones. How are you today?” The woman startles, “Well, you see, I went to put my dog out, and then I was just walking, and couldn’t remember. So it’s all coming full circle, and then I ate a sandwich.” Just then EMS rolls in with another patient, a 75 year-old male coming from home, who was found by his wife in his recliner minimally responsive, with a GCS of 6.  He is followed by a 76 year-old female who had a fall from standing three days ago, and has been increasingly confused today, and is currently oriented only to person.

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Alarms from the ventilator: Troubleshooting high peak pressures

VentilatorAirway management is one of the defining skills of an emergency physician, but our role in the care of intubated patients may continue long after endotracheal tube placement is confirmed. In mechanically ventilated patients, acute elevations in airways pressures can be triggered by both benign and life-threatening causes. When the ventilator alarms, do you know how to tell the difference? What is your approach in troubleshooting the potential problems?

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Supraventricular Tachycardia (SVT) With Aberrancy Versus Ventricular Tachycardia (VT)

2011_04_22AwmEPRDifferentiating between SVT with aberrancy and VT can be very difficult. It is crucial to be able to make this distinction as therapeutic decisions are anchored to this differentiation. Brugada et al prospectively analyzed 384 patients with VT and 170 patients with SVT with aberrant conduction to see if it was possible to come up with a simple criteria to help differentiate between the two with high sensitivity and specificity.

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