Bundle Branch Blocks (BBBs) 101

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).

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By Salim Rezaie, MD|2019-09-10T13:36:03-07:00Aug 29, 2013|Cardiovascular, ECG, Expert Peer Reviewed (Clinical)|

R-Wave Peak Time (RWPT) in Lead II: One Simple Step to Differentiate Wide Complex Tachycardias

There are several algorithms that are currently used to help distinguish Supraventricular Tachycardia (SVT) with aberrancy and Ventricular Tachycardia (VT). Many of these algorithms lack specificity, and let’s face it, who can remember if the absence of an RS complex in the precordial leads is VT or SVT with aberrancy. So what if there was a criterion that had a good sensitivity (SN), specificity (SP), and was one simple step?

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By Salim Rezaie, MD|2019-09-10T13:36:27-07:00Aug 28, 2013|Cardiovascular, ECG|

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

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]

By Michelle Lin, MD|2021-10-06T19:47:10-07:00Aug 27, 2013|ALiEM Cards, Cardiovascular, ECG, Expert Peer Reviewed (Clinical)|

QI Series: Cellulitis vs Necrotizing Fasciitis

Case

A 50-year-old male was referred to the ED for evaluation of cellulitis. The patient had developed pain and swelling in his right groin region 5 days earlier. He had seen his physician 3 days before the ED visit and was started on Doxycycline. On the day of evaluation, he had returned to the office with increasing redness so was referred to the ED.

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By Steven Polevoi, MD|2016-11-11T19:02:57-08:00Aug 26, 2013|Infectious Disease|

Ultrasound-Guided Pericardiocentesis

All the years of ultrasound training in residency has paid off. You found the large pericardial effusion in the hypotensive patient who is still alive, but looks sick. You are a star! The only problem was that you never performed a pericardiocentesis in an awake patient. The cardiology fellow is at home sleeping and/or the closest receiving hospital is about 1 hour away. Now what?

Dr. Arun Nagdev reviews how to do an ultrasound guided pericardiocentesis as part of this new, ongoing series of advanced ultrasound tips for emergency physicians.

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By Arun Nagdev, MD|2022-10-10T14:36:37-07:00Aug 22, 2013|Cardiovascular, Ultrasound|

Choosing the right vasopressor agent in hypotension

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.

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 (β₂agonsim)	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, α_2,β₁, β₂	Increased SVR and inotropy	Tachydysrhythmias and decreased splanchnic flow	Anaphylaxis
Norepinephrine	α₁, α_2,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 β₂effects. 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]

By Todd A. Seigel, MD|2020-07-27T09:44:44-07:00Aug 20, 2013|Critical Care/ Resus, Expert Peer Reviewed (Clinical), Tox & Medications|

Supraventricular Tachycardia (SVT): Are Troponins Necessary?

More than one third of patients will have chest pain associated with SVT causing providers to order troponins and other cardiac enzymes. Elevated troponins are not pathognomonic for CAD/ACS and could represent other etiologies such as sepsis, subarachnoid hemorrhage, and pulmonary embolism. Also, subsequent coronary angiography is not necessary for risk stratification in all cases. SVT causes a rapid heart rate, which is well documented as a cause for modest troponin elevation secondary to cardiac stretch, poor diastolic perfusion, and/or coronary artery vasospasm.

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By Salim Rezaie, MD|2026-06-16T16:03:55-07:00Aug 14, 2013|Cardiovascular|