Alcohol Problems Among Older Adults in the ED

The complications of alcohol use can be subtle in older adults, and the effects of alcohol are often incorrectly attributed to aging. Because of its under-recognition, the barriers to screening, and the many subtle ways in which it can present, some have suggested that alcohol misuse has replaced syphilis as the “great masquerader”. If you don’t think alcohol misuse is a problem among older adults in your ED, it may be because it has been hidden in plain sight.

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

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]

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]

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]

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]

Safe dosing of nebulized lidocaine

Serum lidocaine levels correlate well with observed clinical effects. As the concentration increases, lightheadedness, tremors, hallucinations, seizures, and cardiac arrest can occur. Levels > 5 mcg/mL are associated with serious toxicity. With so many concentrations (1%, 2%, 4%) and routes of administration available, the total dose of lidocaine is always a concern.

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Mythbuster: Calcium Gluconate Raises Serum Calcium as Quickly as Calcium Chloride

LET’S START WITH THE FACTS

We know that calcium chloride (CaCl₂) provides 3 times more elemental calcium than an equivalent amount of calcium gluconate.
So, CaCl₂1 gm = calcium gluconate 3 gm.

CLINICAL QUESTIONS

Does CaCl₂have better bioavailability than calcium gluconate?
Does calcium gluconate have a slower onset of action because it needs hepatic metabolism to release the calcium?

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Patwari Academy videos: Anticoagulation and reversal agents

Bleeding in general is bad. Bleeding while on anticoagulants is VERY bad. Dr. Rahul Patwari reviews the pathophysiology of coagulation, the various reversal agents, and treatment approaches we can use. In this five-part series where all videos are less than 10 minutes, Rahul goes from the basic physiology of coagulation all the way to the complex reasoning and approaches to reversing anticoagulants. These are worth a quick look and review.

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The Dirty Epi Drip: IV Epinephrine When You Need It

You’re a recent graduate picking up an extra shift in a small ED somewhere north of here. At 3 AM an obese 47 year-old woman presents with shortness of breath and difficulty speaking after eating a Snickers bar an hour earlier. She admits to history of hypertension, peanut allergy, and a prior intubation for a similar presentation. She is becoming more obtunded in the resuscitation room as you are collecting your history. A glance at the monitor shows:

HR 130
BP 68/40
O2 saturation 89% on room air

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Must We Avoid Nitrofurantoin with Impaired Renal Function?

Acute uncomplicated cystitis is becoming more difficult to treat in the setting of increasing antimicrobial resistance. In the 2010 IDSA Guideline, as summarized in a PV Card on Cystitis and Pyelonephritis in Women, nitrofurantoin is now listed as the first-line choice, surpassing ciprofloxacin and sulfamethoxazole/trimethoprim from the previous iteration.

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