Derangements in acid-base status are commonly discovered on routine emergency department evaluation and often suggest the presence of severe underlying disease. Many acute conditions can disrupt homeostatic mechanisms used to buffer and excrete acid, and these changes may necessitate immediate intervention. When you discover a patient with an abnormal pH, what is your approach to the diagnosis?
Rob Bryant, MD (@RobJBryant13), Amie Hatch, PharmD, BCPS (@Amie_EMPharmD), and Jeremy Bair, PharmD (@bairpharm) from Intermountain Healthcare in Utah have created and adopted a fantastic medication reference card which is used by physicians and nurses in the Emergency Department. The medications were chosen because they are often prone to dosing errors and require time-sensitive ordering. They generously offered to share this incredibly compact resource for free to the Emergency Medicine community as a PV card. If you see them, give them a high-five.
Intentional overdose patients are notorious for giving inaccurate histories. “I took 14 tablets of this and 8 capsules of that. No, wait. It was 3 tablets of this and a handful of capsules of that… This happened about 2 hours ago. Actually, I think it was last night.” Round and round the merry-go-round we go.
Today, 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.
Recently, 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).
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.
Adapted from [1]
Go to ALiEM (PV) Cards for more resources.
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
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.
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.
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.
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.
| Agent | Primary Receptor | Primary Impact | Potential side effect | Prototypical clinical scenario |
|---|---|---|---|---|
| Phenylephrine | α1 | Increased SVR | Reflexive decreased HR | Neurogenic shock |
| Vasopressin | V | Increased SVR | Decreased splanchnic flow | Adjunct for septic shock |
| Dobutamine | β1, β2 | Increased inotropy | Transient decreases in SVR (β2 agonsim) | Cardiogenic shock from late-stage heart failure |
| Dopamine (low-dose) | D, β1 | Increased inotropy and heart rate | Tachydysrhythmias | Cardiogenic shock, particularly if bradycardic |
| Epinephrine | α1, α2, β1, β2 | Increased SVR and inotropy | Tachydysrhythmias and decreased splanchnic flow | Anaphylaxis |
| Norepinephrine | α1, α2, β1>> β2* | Increased SVR and inotropy | Decreased splanchnic and renal flow | Septic shock |
| Dopamine (high-dose) | D, α1, β1>> β2* | Increased SVR and inotropy | Tachydysrhythmias and decreased splanchnic/renal flow | Bradycardic cardiovascular collapse |
| * Controversial whether norepinephrine and high-dose dopamine have any β2 effects. If any, it is likely very low. | ||||
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