Shock Index: A Predictor of Morbidity and Mortality?

Emergent airway management and severe sepsis are both high-risk situations that are commonly encountered by emergency physicians. It is well known that complications can be high in both situations, which in turn can lead to increased morbidity and mortality. For instance, about 1/4 of patients who are hemodynamically stable prior to intubation get post-intubation hypotension (PIH) after rapid sequence intubation. Also septic patients may not be reliably identified by systemic inflammatory response syndrome (SIRS) markers early in their disease course. The Shock Index (SI) may be an adjunct that is easy to calculate and could predict both PIH and severe sepsis.

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By Salim Rezaie, MD|2019-09-10T13:35:16-07:00Nov 25, 2013|Critical Care/ Resus, Expert Peer Reviewed (Clinical)|

52 Articles in 52 Weeks: Landmark EM Articles 2013

To provide a resource for evidence-based Emergency Medical education, this list of must-read landmark articles was created to supplement the Emergency Medicine (EM) internship year of training. There are 52 articles so that one article can be read at leisure each week of the year. I searched national databases and polled faculty at the University of Washington to identify articles that faculty would expect any EM resident to be familiar with or that they felt were practice-changing in EM. Articles were selected for the final list based on the quality of study design, sample size, and relevance for EM residents.

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By Emily Junck, MD|2017-03-05T14:18:46-08:00Nov 12, 2013|Cardiovascular, Critical Care/ Resus, EMS, Environmental, Gastrointestinal, Infectious Disease, Neurology, Orthopedic, Pediatrics, Pulmonary, Renal, Trauma, Ultrasound|

CPR: Hands-on or Hands-off Defibrillation?

Pauses in chest compressions are known to be detrimental to survival in cardiac arrest, so much so that the 2010 American Heart Association (AHA) emphasize high-quality compressions while minimizing interruptions. There have been some studies that now advocate for continuous chest compressions during a defibrillation shock. There have been substantial changes to external defibrillation technology including:

Biphasic shocks with real-time impedance monitoring to reduce peak voltages
Paddles being replaced by adhesive pre-gelled electrodes
Enhancement in ECG filtering permitting rhythm monitoring during chest compressions.

So the mantra of “hard and fast” may be true when it comes to CPR, but the real question now becomes, should we be continuing CPR during defibrillation?

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By Salim Rezaie, MD|2019-09-10T13:35:23-07:00Oct 28, 2013|Cardiovascular, Critical Care/ Resus, Expert Peer Reviewed (Clinical)|

Mechanical vs Manual CPR Chest Compressions

When talking about Out of Hospital Cardiac Arrest (OHCA) there are really only three things that make a true difference on outcomes (i.e. survival and neurologic function):

High quality, non-interrupted CPR
Early defibrillation
Therapeutic hypothermia

The quality of CPR is often under appreciated and performed incorrectly (too slow and/or not hard enough). With mechanical CPR, chest compressions are delivered uninterrupted and at a predefined depth and rate. In my own practice I have seen these devices being used more and more, but my questions is do these devices impact outcomes?

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By Salim Rezaie, MD|2019-09-10T13:35:31-07:00Oct 23, 2013|Cardiovascular, Critical Care/ Resus|

Treating Ischemic Stroke with tPA in the ED: Time is Brain

Ischemic stroke is an emergent and devastating neurologic disorder, and is a leading cause of both death and disability in the United States. With each minute of brain ischemia, two million neurons are irreversibly damaged. Total ischemic time is linked to functional outcome, and therefore, the role of the Emergency Department is paramount in the management of these patients. Fibrinolytic therapy has become a mainstay of therapy for acute stroke, but guidelines for the use of tPA are dynamic, and often even controversial. When you identify someone with symptoms of stroke, what is your approach to determining if a patient should receive tPA?

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By Todd A. Seigel, MD|2016-11-11T19:04:15-08:00Oct 10, 2013|Critical Care/ Resus, Expert Peer Reviewed (Clinical), Neurology|

Deciphering Acid-Base Disorders

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?

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By Todd A. Seigel, MD|2016-12-14T05:13:55-08:00Sep 16, 2013|Critical Care/ Resus, Expert Peer Reviewed (Clinical)|

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|