Discover common practices that persist in the hospital wards despite no proven benefit! We review how potassium replacement goals should not drive you bananas, extra oxygen should not give you comfort, and how you should maybe calm down with antipsychotics for delirium. Join returning guests: high-value care specialist Dr. Lenny Feldman (@DocLennyF, Johns Hopkins) and tweetorialist Dr. Tony Breu (@tony_breu, Harvard) as they walk us through round 3 of “Things We Do for No ReasonTM (TWDFNR 3).
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Written and Produced by: Burton H. Shen MD, Justin Berk, MD MPH MBA
Hosts: Justin Berk MD MPH MBA; Stuart Brigham MD; Matthew Watto MD, FACP; Paul Williams MD, FaCP
Editor: Matthew Watto MD, FACP (written materials); Clair Morgan of Nodderly.com (audio)
Guest: Lenny Feldman MD, Tony Breu MD
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Started in 2012 at SHM Annual Meeting, “Things We Do For No Reason™” was a talk that covered 3 – 4 new topics each year representing “the low hanging fruit of high value care.” Topics include practices that have no evidence behind them, don’t help patients, and are things we should, for the most part, get rid of. These topics have now become a regular series in the Journal of Hospital Medicine. The goal is for learners to become more skeptical and question norms rather than accept practices without evidence.
Check out this Master Index with all the Choosing Wisely / TWDFNR articles!
TWDFNR Article – Potassium Replacement (publication pending)
Dr. Feldman’s expert opinion: 3.5-5.0 mEq/L
European Resuscitation Council Guidelines in 2015 said there is no universal definition for hyperkalemia. They defined hypokalemia as <3.5 and hyperkalemia as >5.5
There are not great guidelines for electrolyte replacement patients who present with an acute myocardial infarction, despite being almost universally taught, that acute MI patients should have potassium level greater than 4.0. 2017 AHA/ACC/HRS guidelines centered around preventing ventricular fibrillation or ventricular tachycardia with a “normal” potassium level.
Studies that have looked at admission potassium level showed increased risk of ventricular arrhythmias if the admission potassium was low [Patel 2017].
The National Council on Potassium in Clinical Practice recommends a target of 4.0 or higher in patients with heart disease who are at risk for serious ventricular tachyarrhythmias [Cohn, 2000]. No major organizations clearly state what the goal should be after an acute MI.
Potentially, death. Dr. Feldman shared an anecdote of having a patient die when he was replacing potassium (intravenously) for a potassium under 4.
A retrospective observational study that looked at admission and mean potassiums for about 38,000 patients with acute MI from 2000 to 2008 across 67 hospitals. The end points were arrhythmias AND mortality. They found that mean potassium levels between 3.5 and 4.0 had the lowest mortality. Mean potassium below 3.5 was associated with increased mortality and mean potassium above 4.5 was also associated with increased mortality [Goyal, 2012].
Dr. Breu’s expert opinion: Low potassium could cause arrhythmias, but could also be a confounder. Low potassium could indicate high levels of catecholamines that might be causing the arrhythmia, rather than the low potassium being the cause.
Dr. Feldman’s expert opinion: Patients with acute MI with a potassium between 3.0 to 3.5 should receive potassium replacement. Based on observational data, potassium of 3.5-4.0 is a good goal. Do not try to push K+ above 4.4. For other internal medicine patients, 3.5-4.0 seems to be a reasonable goal, but this is all based on observational data.
Dr. Breu’s expert opinion: For patients with acute MI, acute heart failure, and cirrhosis at risk for hepatic encephalopathy, the goal is over 3.5; otherwise, patients with potassium over 3.0 is acceptable.
As supplemental O2 increases for patients, it increases pO2 well, but does not increase total oxygen content. If pO2 increases from 100 to 500 mm Hg, the total oxygen content has increased only 6%. Even though pO2 goes up by five times, the actual content increases only 6%. Increasing supplemental does not increase oxygen to the tissues by that much. The sensors in the body react to pO2, not total oxygen content [Loscalzo, 2017].
When pO2 increases, the reaction by the vessels (with the exception of the lungs) is to vasoconstrict because oxygen free radicals are toxic. The body vasoconstricts to protect the tissue from the free radicals of oxygen. This decreases the delivery of blood to the tissues [Collins, 2015].
James Lorrain Smith put birds in chambers with increasing oxygen content that showed the toxic effects of oxygen [Smith, 1899]. Dr. Breu cited multiple studies from the 1940s that show increased oxygen causes vasoconstriction of the arteries feeding the brain and the coronary arteries.
A randomized control trial (by the AVOID investigators) looked at patients with a myocardial infarction with an O2 saturation of 94% and randomized them to either eight liters of supplemental oxygen or no supplemental oxygen. The patients randomized to the supplemental oxygen group had an increased risk of recurrent MI and a larger infarct size [Stub, 2015].
The IOTA systematic review and meta-analysis, found that acutely ill patients with O2 saturations above 96% had increased in-hospital mortality [Chu, 2018].
Patients who have acute COPD exacerbation are at risk of becoming hypercarbic. The physiology is often cited as the “loss of hypoxic drive,” which plays a role, but according to Dr. Breu, it is likely the loss of hypoxic vasoconstriction in the lung that probably contributes more to the hypercarbia.
“Worsening ventilation-perfusion matching and the Haldane effect (decreased affinity of hemoglobin for carbon dioxide as the PaO2 rises), rather than the previously theorized decrease in hypoxic drive, are now believed to contribute most to hyperoxia-induced hypercarbia.” –TWDFNR (Moss, 2019)
Per the BMJ Practice Recommendations: the strongest recommendations are for patients with acute MI and acute stroke. Do not give supplemental oxygen if O2 saturation is above 92% (strong recommendation) or above 90% (weak recommendation). For all other patients, there is no recommendation for a lower limit, but stop or turn down supplemental oxygen for oxygen saturation over 96% [Siemieniuk, 2018].
Dr. Breu’s expert opinion: Do not start supplemental oxygen for patients with >90% O2 saturation or >88% for COPD patients. Turn down or stop supplemental oxygen for O2 saturation over 96%.
Delirium is an acute change in cognition that is almost always characterized by inattention, and typically associated with disordered thinking and/or alterations in consciousness.
Dr. Feldman suggests that the pre-test probability for delirium for admitted patients is about 33%. He recommends asking “what day of the week is it?” and asking the patients to recite the months backwards. These are tests with good sensitivity (93%)[Fick 2015]. Another test developed for diagnosing delirium is the 3D-CAM test [Marcantonio, 2014].
Not benzodiazepines (unless the patient is in alcohol withdrawal), not acetylcholinesterase inhibitors, and not antipsychotics based on the larger meta-analyses [Lonergan, 2009, Yu, 2018, Burry, 2018]. A few studies have shown some positive results from antipsychotics quetiapine and haloperidol, but the data is not strong [Tahir, 2010, Kalisvaart, 2005].
“The prescribing practitioner should not prescribe antipsychotic… medications for the treatment of older adults with postoperative delirium who are not agitated and threatening substantial harm to self or others.”The American Society of Geriatrics https://www.ncbi.nlm.nih.gov/pubmed/25495432
Dr. Feldman’s expert opinion: Remove IVs if they are not needed. If they need the IV, tape the tubing with gauze from the wrist to the shoulder and have the attached tubing exit behind the shoulder. Don’t draw blood if you don’t need to. Don’t take vital signs if you don’t need to. Get rid of problematic medications. Correct any metabolic disturbances. Let the patient sleep. Get them private rooms to help them sleep. Get the patients mobile. Treat pain if applicable.
Listeners will be able to explain the target potassium levels for patients with acute MI and acute heart failure, target goals for O2 saturation, and the evidence of why antipsychotics do not work well for delirium.
After listening to this episode listeners will…
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Dr. Feldman and Dr. Breu report no relevant financial disclosures. The Curbsiders report no relevant financial disclosures.
Feldman L, Breu T, Shen BH, Berk JL, Williams PN, Brigham SK, Watto MF. “#195 TWDFNRTM 3: Potassium, Oxygen, and antipsychotics”. The Curbsiders Internal Medicine Podcast. http://thecurbsiders.com/episode-list. February 17, 2020.
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