Question Of The Day #21

question of the day
qod21

Which of the following is the most appropriate next step in management for this patient’s condition?

This patient experienced a witnessed cardiac arrest at home, after which pre-hospital providers initiated cardiopulmonary resuscitation (CPR, or “chest compressions”) and Advanced Cardiovascular Life Support (ACLS). ACLS includes the tenets of Basic Life Support (BLS), such as early initiation of high-quality CPR at a rate of 100-120 compressions/minute, compressing the chest to a depth of 5 cm (2 inches), providing 2 rescue breaths after every 30 compressions (30:2 ratio), avoiding interruptions to CPR, and allowing for adequate chest recoil after each compression. In the ACLS algorithm, intravenous epinephrine is administered every 3-5 minutes and a “pulse check” is performed after every 2 minutes of CPR. The patient’s cardiac rhythm, along with the clinical history, helps decide if the patient should receive defibrillation (“electrical shock”) or additional medications. The ACLS algorithm divides management into patients with pulseless ventricular tachycardia (pVT) or ventricular fibrillation (VF) and patients with pulseless electric activity (PEA) or asystole.

The cardiac rhythm seen during the pulse check for this patient is a wide complex tachycardia with a regular rhythm. In the setting of cardiac arrest, chest pain prior to collapse, and a history of acute coronary syndrome, ventricular tachycardia is the most likely cause. The ACLS algorithm advises unsynchronized cardioversion at 150-200 Joules for patients with pVT or VF. Watching the cardiac monitor for a rhythm change (Choice A) or checking for a pulse (Choice D) are not recommended after defibrillation. A major priority of both BLS and ACLS is to avoid interruptions to CPR, so the best next step in management is to continue CPR (Choice B) after defibrillation. Administration of intravenous adrenaline (Choice C) is helpful for cardiac arrests to initiate shockable rhythm and should be repeated every 3-5 minute or every 2 cycle of CPR, particularly valuable in asystole patients. Calcium gluconate is another drug that can be used in patients with hyperkalemia and indicated in a patient with known kidney disease, missed hemodialysis sessions, or a history of usage of medications that can cause hyperkalemia. Magnesium can be used for patients who show polymorphic VT, particularly Torsades de Pointes. The next best step in this scenario is to continue CPR, regardless of the etiology of the cardiac arrest. Correct Answer: B.

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #21," in International Emergency Medicine Education Project, November 13, 2020, https://iem-student.org/2020/11/13/question-of-the-day-21/, date accessed: November 25, 2020

Push Th(d)ose Vasopressors

Push Th(d)ose Vasopressors

Background

Since Scott Weingart first advocated for using push-dose pressors in the Emergency Department (ED) over a decade ago(1), push-dose vasopressors, also known as bolus-dose vasopressors have seemingly found their way into many EDs. However, recent studies have sought to ask more questions regarding its use and safety in the Emergency Department.

Vasopressors such as epinephrine and norepinephrine are commonly used for regulating and maintaining adequate blood pressure or mean arterial pressure (MAP). While these are usually administered as a continuous infusion via central access, administering them as a small bolus through peripheral access came to be known as push-dose vasopressor in practice.

Traditionally, this small bolus strategy was used in the operating room (OR) by anesthetists to treat transient hypotension due to sedating agents or spinal anesthesia. Multiple studies have supported the safety and efficacy of push-dose vasopressors in this clinical setting/patient population (2).

Swensen, et al. (3) studied the safety of bolus-dose phenylephrine for hypotension in the Emergency Department, however, data on the efficacy and safety of push-dose pressors remains sparse in ED and in-patient settings. Studies published in the past few years have questioned the lack of evidence regarding the safety and efficacy of push-dose pressor use in ED settings and highlighted some negative consequences of its use (4). To understand the concerns, it’s important we first understand the vasopressors, indications for use, and preparation in the ED.

Push-dose pressors in the Emergency Department

The two common vasopressors used as push-dose pressors in the Emergency Department are Epinephrine and Phenylephrine. Patients needing emergency airway, traumatic brain injury, and post-cardiac arrest with the return of spontaneous circulation may all experience hypotension which could lead to adverse outcomes. Push-does pressors have been proposed as a temporary measure to limit the hypotension while a vasopressor infusion/definitive treatment is being set up (5).

phenilephrine vs epinephrine
push dose epinephrine
push dose phenilephrine

Clinical settings in the ED where the use of push-dose pressor is proposed:

  1. Airway management: Hypotension prior, during, and post-intubation could be treated with bolus-dose vasopressors. Panchal et al. (6) did a retrospective chart review of intubated hypotensive patients in which phenylephrine was used. Bolus-dose phenylephrine demonstrated an increase in systolic blood pressure and the authors recommended further studies to understand the best use of phenylephrine for post-intubation hypotension.
  2. Return of spontaneous circulation (ROSC): In patients with ROSC, bolus-dose pressors may aid in the maintenance of end-organ perfusion, which is often impaired after ROSC (7).
  3. Traumatic brain injury: By rapidly increasing mean arterial pressure and thus cerebral perfusion pressure, bolus-dose vasopressors may help to prevent secondary brain injury.

What are the concerns regarding the use of push-dose pressors in the ED?

Acquisto and Bodkin (8) cited a few dosing errors while using push-dose pressors and highlighted that emergency physicians are less familiar with the practice of medication preparation/manipulation and hence dosing errors are expected, inadvertently causing patients more harm than benefit. They also emphasized on the lack of evidence in the literature regarding the efficacy and safety of push-dose pressors in a stressful environment like the ED.

Rotando and Picard et al. (9) in their prospective observational study of 146 patients receiving push-dose pressors in the ICU had thirteen (11.2%) patients have a dose-related medication error and seventeen (11.6%) adverse events. They concluded while push-dose pressors where efficacious, they were associated with adverse drug events and medication errors.

Cole et al (10). performed a retrospective analysis of 249 patients receiving push-dose pressors and found a higher incidence of adverse hemodynamic effects (39%) and human errors (19%). They emphasized the need for further studies to question whether push-dose pressors improve outcomes, and if so, how to safely implement them in practice.

Another concern raised is whether physicians may bypass standard resuscitation practices of fluid boluses in favor of using push-dose pressors. Schwartz et al. (11) found that only 34% of patients received an appropriate fluid challenge before using push-dose pressors in a retrospective chart review of 73 patients receiving push-dose pressors for acute hypotension in the ED. Furthermore, it appeared that patients who did not receive an appropriate fluid bolus needed more doses of bolus-dose pressors followed by the need for continuous vasopressor infusion within 30 minutes of bolus-dose pressor use.

Emergency physicians work in stressful environments which raises concerns on the ability of the physician to perform accurate dose calculations under duress (4). The prepared syringe also contains multiple individual doses, and using more concentrated solutions potentially increases the risk of overdose and extravasation injury (12).

Conclusion

While the practice of using push-dose pressors has found its way into the Emergency Department, it is crucial to acknowledge that evidence regarding its safety and benefits is limited. However, rather than disregarding the practice, high-quality research should be encouraged, which could potentially be practice-changing. Holden et al. (12) offer a framework of operational and safety considerations for the use of push-dose pressors in the ED and is a must-read for all using push-dose pressors in their current practice.

References

  1. Scott Weingart. EMCrit Podcast 6 – Push-Dose Pressors. EMCrit Blog. Published on July 10, 2009. Accessed on September 25th 2020. Available at [https://emcrit.org/emcrit/bolus-dose-pressors/ ].
  2. Lee A, Ngan Kee WD, Gin T. A quantitative, systematic review of randomized controlled trials of ephedrine versus phenylephrine for the management of hypotension during spinal anesthesia for cesarean delivery. Anesth Analg. 2002 Apr;94(4):920-6, table of contents. doi: 10.1097/00000539-200204000-00028. PMID: 11916798.
  3. Swenson K, Rankin S, Daconti L, Villarreal T, Langsjoen J, Braude D. Safety of bolus-dose phenylephrine for hypotensive emergency department patients. Am J Emerg Med. 2018 Oct;36(10):1802-1806. doi: 10.1016/j.ajem.2018.01.095. Epub 2018 Feb 19. PMID: 29472039.
  4. Cole JB. Bolus-Dose Vasopressors in the Emergency Department: First, Do No Harm; Second, More Evidence Is Needed. Ann Emerg Med. 2018 Jan;71(1):93-95. doi: 10.1016/j.annemergmed.2017.05.039. Epub 2017 Jul 26. PMID: 28754354.
  5. Weingart S. Push-dose pressors for immediate blood pressure control. Clin Exp Emerg Med. 2015;2(2):131-132. Published 2015 Jun 30. doi:10.15441/ceem.15.010
  6. Panchal AR, Satyanarayan A, Bahadir JD, Hays D, Mosier J. Efficacy of Bolus-dose Phenylephrine for Peri-intubation Hypotension. J Emerg Med. 2015 Oct;49(4):488-94. doi: 10.1016/j.jemermed.2015.04.033. Epub 2015 Jun 20. PMID: 26104846.
  7. Gottlieb M. Bolus dose of epinephrine for refractory post-arrest hypotension. CJEM. 2018 Oct;20(S2):S9-S13. doi: 10.1017/cem.2016.409. Epub 2017 Jan 10. PMID: 28069098.
  8. Acquisto NM, Bodkin RP, Johnstone C. Medication errors with push dose pressors in the emergency department and intensive care units. Am J Emerg Med. 2017 Dec;35(12):1964-1965. doi: 10.1016/j.ajem.2017.06.013. Epub 2017 Jun 7. PMID: 28625533.
  9. Rotando A, Picard L, Delibert S, Chase K, Jones CMC, Acquisto NM. Push dose pressors: Experience in critically ill patients outside of the operating room. Am J Emerg Med. 2019 Mar;37(3):494-498. doi: 10.1016/j.ajem.2018.12.001. Epub 2018 Dec 3. PMID: 30553634.
  10. Cole JB, Knack SK, Karl ER, Horton GB, Satpathy R, Driver BE. Human Errors and Adverse Hemodynamic Events Related to “Push Dose Pressors” in the Emergency Department. J Med Toxicol. 2019 Oct;15(4):276-286. doi: 10.1007/s13181-019-00716-z. Epub 2019 Jul 3. PMID: 31270748; PMCID: PMC6825064.
  11. Schwartz MB, Ferreira JA, Aaronson PM. The impact of push-dose phenylephrine use on subsequent preload expansion in the ED setting. Am J Emerg Med. 2016 Dec;34(12):2419-2422. doi: 10.1016/j.ajem.2016.09.041. Epub 2016 Sep 22. PMID: 27720568.
  12. Holden D, Ramich J, Timm E, Pauze D, Lesar T. Safety Considerations and Guideline-Based Safe Use Recommendations for “Bolus-Dose” Vasopressors in the Emergency Department. Ann Emerg Med. 2018 Jan;71(1):83-92. doi: 10.1016/j.annemergmed.2017.04.021. PMID: 28601272.
Cite this article as: Neha Hudlikar, UAE, "Push Th(d)ose Vasopressors," in International Emergency Medicine Education Project, November 11, 2020, https://iem-student.org/2020/11/11/push-thdose-vasopressors/, date accessed: November 25, 2020

More Posts From Dr. Hudlikar

The EKG Case of No Symptoms

the ecg case of no symptoms

Case Presentation

A 52-year-old woman presents to the ED from an outpatient dialysis center with a rather vague history. She has no symptoms and feels normal, but she was told something “was either too low or too high” on her vital signs at dialysis, so dialysis staff did not perform her scheduled dialysis session. No one had called ahead to alert the emergency department, and the patient had driven herself to the ED, as she was instructed. Vitals show a normal temperature, respiratory rate, oxygen saturation, blood pressure of 102/47 mm Hg, and a heart rate of 138 beats per minute. The physical exam is normal besides a mild regular tachycardia and a working AV dialysis fistula on the right arm. EKG is done, and a representative portion is shown below:

EKG from the prior year is shown for comparison.

How would you interpret the first EKG, and what are your next steps?

Discussion

While you are thinking, I will discuss a few of my practical observations from working in the pit. I want to focus not so much on the diagnosis but on working with these types of scenarios.

Treat the patient and not the chief complaint, vitals, labs, EKGs, studies, or referral information.

When they are feeling great and have no symptoms, they are feeling great and have no symptoms! Your nurses will not necessarily think this way, but one does not feel great while having a real STEMI apparent on the triage EKG. So what is it then, if the patient is here for a contact lens stuck in their eye, but has an EKG STEMI? Worst case – a prior STEMI that never corrected or evolved on the EKG. A ventricular aneurysm? Leads misplaced? Did your EKG tech do an EKG on themselves? A silent MI can occur, but an incidental STEMI is unlikely. 

Of course, the patient has to be alert, competent, and not intoxicated. They should not be lying about or hiding their symptoms and should not have a secondary interest like the need to make it to a daughter’s wedding - live or die. The easiest thing is to ask directly.

What is the rhythm's rate doing when it is left alone?

Afibs and MATs will tend to vary greatly in the second to second heart rate, sinus tachycardias will fluctuate some, while A-flutters and SVTs will tend to stick to a single number no matter what you do and no matter if the patient is walking, talking, or snoozing. Stable Vtachs will depend on a number of factors like being monomorphic or polymorphic – but we are talking about narrow QRS dysrhythmias or ones with an obvious bundle. 

So if you cannot tell from the EKG – observe what the thing does while left alone. As long as the patient is otherwise stable or has had symptoms for a while, you have some time.

Adenosine – not just for SVT conversion

“SVT = adenosine” should not be an automatic equation. First of all, there are contraindications to adenosine based on past history or current medications taken. But adenosine can also be used to “stretch out” weird or equivocal fast rhythms to make flutter waves or hidden P waves come out, so you can see and diagnose the arrhythmia vs. sinus. 

You have to have continuous EKG recording going or printing the monitor strip to spot the temporary effect.

Hypotension + tachy-dysrhythmia: does not necessarily add up to Joules.

The textbook mantra of shocking any dysrhythmia associated with hypotension does not hold up in reality. In reality, you will find that most of your Afibs with a rapid response, your new-onset atrial flutters and your SVTs will have a lousy blood pressure: systolic of 80s and 90s are almost to be expected, and may even dip down to 70s on occasion. It also depends on a prior BP baseline, if the person is petite or dehydrated. But if the patient is mentating well and is not suffocating or experiencing crushing chest pain with diaphoresis, please don’t feel like you have to shock them. The body is not used to the new arrhythmia, and the rapid rate compromises the cardiac output. 

Yes, you can still use your rate and rhythm controllers. Give the patient a gentle fluid bolus if you must. Of course, pacer pads do have to be on ahead of time.

Be afraid of shocking dialysis patients. Check electrolytes.

Hypotension with normal mentation is much better than a PEA arrest. Shocking extremes of electrolyte and acid/base abnormalities, whether due to TCA and other overdoses or in dialysis patients, will give you exactly that. This is especially true for the so-called “slow-X” arrhythmias: slow Afib, slow SVT, or even V-slow (Vtach with a rate of 130) that dialysis patients like to present in. 

Just like airplane travel in transportation, electricity is in general the safest rhythm conversion strategy. But there are exceptions, and you only need to crash once.

A-flutter and the stuck rate of 150

You already know this, but just as a reminder. If the rate is a steady 150, plus or minus, and it is stuck there, you should think of atrial flutter. 

Even if you do not see obvious classic flutter waves, there is a high chance of 2:1 conduction. In this case, I thought of it. Fortunately, it did not think of me.

Adenosine (again)….the 6, the 12…the 24??

Sometimes adenosine is not pushed correctly, but sometimes it just does not work or only works for a few seconds. Sometimes the patient’s Mom knows best what works, so you should listen. Sometimes the last time it was used, the patient really did feel like they were going to die – so they do not ever want it again. Ever. That you should try 6mg, then 12mg, then stop is generally true, but it is also a dead-end. What is your back up plan? Electricity? In the past I have given the doses in reverse, combined 6mg with the Valsalva maneuver and had given a preemptive beta-blocker or calcium channel blocker dose 10-15 minutes before adenosine to massage a stubborn heart into adenosine submission. It is ok to experiment a little. Another practical point – how much does your ED freak an SVT patient out while he or she is being triaged and roomed? I still do not completely understand why an SVT tends to be rushed up in the same fashion as a STEMI with cardiogenic shock and bradycardia, judging from staff adrenaline levels. 

Calm the patient down, turn the lights off and let them change. It's like a kid with croup. Remember, it is lack of the sympathetic influx that we want, not an excess. Otherwise, why try the Valsalva at all? Has anyone attempted a stellate ganglion block Vfib-style for a refractory SVT? An overkill, I know….but could be fun, and practice for the real deal.

Aren’t all AVNRTs verapamil sensitive?

Years ago, in my first year of solo practice, I had a case of a refractory SVT in a young teenager, which a pediatric cardiologist consulting by phone called a “verapamil-sensitive AVNRT” based on the EKG alone. I was impressed. Hours later, I decided to flash my newly acquired cool knowledge and relayed the same to my in-house cardiologist, who looked at me with a grin and a raised eyebrow and said, “Anthony, all AVNRTs are verapamil sensitive”. At that time, I was also sensitive, and so my feelings were hurt. Lately I have gotten into the habit of treating my SVTs with diltiazem – as a purer verapamil relative. With generally good results and no need to stand in front of the patient during administration by the nurse. 

The bottom line is – you have choices. Especially, if the patient is already on a beta-blocker or a calcium channel blocker, give them a beta or a calcium blocker IV, see what happens.

Case Concluded

Despite a single nadir of blood pressure of 75 systolic, the rest holding steadily in the high 90s, the patient received a single dose of IV diltiazem and a small IV fluid bolus. Labs reviewed prior showed normal potassium, calcium, sodium, magnesium and the rest of them. Her average heart rate reduced to about 106 and a repeat EKG is shown, accidentally capturing an event: 

She, of course, had a “verapamil sensitive” SVT. The patient’s new right bundle block had also improved to an incomplete, proving to be either SVT- or rate-related. The patient had never experienced any symptoms while in the ED. She was observed for a short time, scheduled for an out-of-sequence dialysis the next day and discharged home with a normal heart rate. I guess, in this case, we did treat the EKG and not the patient.

Cite this article as: Anthony Rodigin, USA, "The EKG Case of No Symptoms," in International Emergency Medicine Education Project, October 26, 2020, https://iem-student.org/2020/10/26/the-ekg-case-of-no-symptoms/, date accessed: November 25, 2020

Want to read more, take a look this post from September

Question Of The Day #18

question of the day
qod18
839 - diffuse ST elevation - pericarditis?

Which of the following is the most appropriate next step in management for the patient’s condition?

This patient presents to the emergency department with signs and symptoms consistent with acute pericarditis from a likely viral etiology. Common causes of acute pericarditis include idiopathic, infectious (viral, bacterial, or fungal), malignancy, drug-induced, rheumatic disease-associated (lupus, rheumatoid arthritis, etc.), radiation, post-MI (Dressler’s Syndrome), uremia, and severe hypothyroidism. The chest pain associated with this diagnosis is typically worse with supine positioning, improved with sitting forward, worse with inspiration, and may radiate to the back. A pericardial friction rub may be heard on auscultation of the chest, and there may be a low-grade fever on the exam. The hallmark EKG demonstrates diffuse ST-segment elevation with PR segment depression, although normal ST segments or T wave inversions can be seen on EKG later in the disease process. The treatment of acute pericarditis depends on the underlying cause of the disease. This patient has likely viral pericarditis with no clinical signs of myocarditis (i.e. fluid overload, cardiogenic shock, etc.) or cardiac tamponade (i.e. obstructive shock, distended neck veins, muffled heart sounds, low voltage QRS complexes or electrical alternans on EKG). A cardiac sonogram would be prudent to evaluate for a pericardial effusion. This patient’s disease course likely will resolve with NSAIDs in 1-2 weeks. Ibuprofen (Choice C) is the preferred treatment over aspirin (Choice A) or steroids (Choice B). Colchicine (Choice D) can be useful in recurrent episodes of pericarditis to reduce recurrence and in acute pericarditis not responding to NSAIDs. Correct Answer: C 

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #18," in International Emergency Medicine Education Project, October 23, 2020, https://iem-student.org/2020/10/23/question-of-the-day-18/, date accessed: November 25, 2020

You may want to read these

Question Of The Day #17

question of the day
qod17

Which of the following is the most likely cause for the patient’s elevated cardiac troponin level in the emergency department?

Elevated cardiac troponin levels, or troponinemia, are one sign that the myocardium may be infarcting or under some type of stressful condition. Cardiac troponin levels are assessed in conjunction with the clinical history, physical exam, EKG, and another laboratory testing in deciding if troponinemia is due to cardiac ischemia or another condition. Conditions associated with elevated cardiac troponin levels include cardiac ischemia (i.e. STEMI, NSTEMI), cardiac contusion, cardiac procedures, congestive heart failure, renal failure, aortic dissection, tachy- or bradyarrhythmias, rhabdomyolysis with cardiac injury, Takotsubo syndrome, pulmonary embolism, acute stroke, myocarditis, sepsis, severe burns, extreme exertion, and other conditions. It is unlikely that this patient had elevated troponin levels from Acute coronary syndrome (Choice D) as her cardiac catheterization results showed no significant occlusive lesions in the coronary arteries. D-Dimer levels do increase with patient age, but cardiac troponin levels do not increase with patient age (Choice B). Sepsis (Choice C) is a cause for elevated troponin levels, but this patient has no clinical signs or sepsis symptoms. Atrial fibrillation with a rapid rate (Choice A) is the most likely cause of this patient’s elevated troponin level. Correct Answer: A 

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #17," in International Emergency Medicine Education Project, October 16, 2020, https://iem-student.org/2020/10/16/question-of-the-day-17/, date accessed: November 25, 2020

You may want to read these

Question Of The Day #16

question of the day
qod16

Which of the following is the most appropriate next step in management for this patient’s condition?

This patient sustained a penetrating traumatic injury to the left chest and presented to the emergency department with hemodynamic instability (tachycardic and hypotensive). Some differential diagnoses to consider on arrival include tension pneumothorax, cardiac tamponade, aortic injury, or aero-digestive tract injury. Prior to taking a detailed history on any trauma patient, a primary survey should be performed. The goal of the primary survey in a trauma patient is to identify and treat any life-threatening injuries as soon as possible. The primary survey is also known as the “ABCs.” Sometimes it is referred to as the “ABCDEFs.” This acronym stands for Airway, Breathing, Circulation, Disability, Exposure, and FAST exam (How to learn eFAST exam for free). Each letter is addressed and assessed in the order they exist in the alphabet. This creates a methodical, algorithmic approach to assist the practitioner in assessing the trauma patient for life-threatening injuries. The sonographic view shown in this question is the subxiphoid (cardiac) view and demonstrates the presence of free fluid. Free fluid on ultrasound appears black, or “anechoic” and is assumed to be blood in the setting of trauma. The free fluid is highlighted by red stars in the image below. The collapse of the right ventricle is shown by the yellow arrow in the below image.

cardiac tamponade - explained
SS Video 3 Pericardial Tamponade

In conjunction with hemodynamic instability and a history of penetrating chest trauma, this sonographic view strongly supports the diagnosis of cardiac tamponade. Consulting the general surgery team for exploratory laparotomy (Choice A) would be the correct course of action for a patient with hemodynamic instability and free fluid on the other abdominal views of the FAST exam. Needle decompression of the chest (Choice B) would be the correct initial treatment for a tension pneumothorax. The patient described in the case has clear bilateral lung sounds, no tracheal deviation mentioned, normal O2 saturation on room air, and sonographic demonstration of cardiac tamponade. A CT scan of the chest, abdomen, and pelvis (Choice D) would be indicated in this patient if he had normal vital signs and no free fluid on the FAST exam. A pericardiocentesis (Choice C) is the most appropriate next step in the management of this patient with cardiac tamponade to relieve signs of obstructive shock. It should be noted that this procedure has limitations and is not always effective. Pericardiocentesis is a temporizing treatment with pericardiotomy being the definitive therapy. Blood in an acute hemopericardium may clot and be unable to be aspirated with a large-bore needle. The procedure may injure surrounding organs, such as the liver, intestines, or heart itself. Ultrasound-guidance should be used whenever possible to avoid injury to surrounding organs. Emergent thoracotomy to relieve the cardiac tamponade should be performed on any patient with confirmed cardiac tamponade and cardiac arrest in the Emergency Department. Correct Answer: C

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #16," in International Emergency Medicine Education Project, October 9, 2020, https://iem-student.org/2020/10/09/question-of-the-day-16/, date accessed: November 25, 2020

You may want to read these

Question Of The Day #15

question of the day
qod 15 - pleuritic chest pain

Which of the following is the best course of action to further evaluate for a diagnosis of pulmonary embolism?

Pulmonary embolism (PE) is a potentially lethal diagnosis evaluated by a combination of a thorough history, physical exam, and the use of risk stratification scoring tools. The Wells criteria and the PE rule-out criteria (PERC) are two well-accepted risk stratification tools for PE. These criteria are each listed below (Wieters et al., 2020).

Wells’ Criteria for Pulmonary Embolism

CriteriaPoint Value
Clinical signs and symptoms of DVT+3
PE is #1 diagnosis, or equally likely+3
Heart rate > 100+1.5
Immobilization at least 3 days, or Surgery in the Previous 4 weeks+1.5
Previous, objectively diagnosed PE or DVT+1.5
Hemoptysis+1
Malignancy w/ Treatment within 6 mo, or palliative+1
Interpretation
Score >4 = High probability
Score 2–4 = Moderate probability
Score <2 = Low probability

Pulmonary Embolism Rule Out Criteria

All Variables Must Be Present for <2% Chance of PE
Pulse oximetry >94% (room air)
HR <100
No prior PE or DVT
No recent surgery or trauma within prior 4 wk
No hemoptysis
No estrogen use
No unilateral leg swelling
The patient in this clinical vignette would have a Wells score of 1.5 (low risk) due to her persistent tachycardia of unknown etiology. The PERC rule can not be applied to this patient as she is over 50-years-old and has tachycardia. If the patient was low risk on Wells score and meet all the PERC rule criteria, she would have a less than 2% likelihood of her symptoms being due to a PE. It is important to note that only patients with a low-risk Wells score (low pretest probability for PE) can be subjected to the PERC rule. A low-risk Wells score (<2) is investigated with a D-Dimer test (Choice B), while moderate to high-risk Wells scores are investigated with a CT Pulmonary Angiogram (CTPA) (Choice C). A V/Q Scan (Choice A) is not a first-line test for the diagnosis of PE as it is less sensitive than a CTPA scan. Unlike a CTPA scan, a V/Q scan may be nondiagnostic in the setting of lung consolidation, effusions, or other airspace diseases. V/Q scans are second-line tests to CTPA when there are contraindications to a CTPA (i.e., renal failure). Lorazepam (Choice D) is a benzodiazepine that may be helpful in reducing tachycardia, which is secondary to anxiety. However, this therapy does not help further discern if the patient may have a PE. Correct Answer: B 

References

Wieters J, McDonough J, Catral J. Chest Pain. In: Stone C, Humphries RL. eds. CURRENT Diagnosis & Treatment: Emergency Medicine, 8e. McGraw-Hill; Accessed August 17, 2020. https://accessmedicine.mhmedical.com/content.aspx?bookid=2172&sectionid=165059275

Nickson, C. (2019). Pulmonary Embolism. Life in the Fastlane. Accessed on August 17, 2020. https://litfl.com/pulmonary-embolism/

Cite this article as: Joseph Ciano, USA, "Question Of The Day #15," in International Emergency Medicine Education Project, October 2, 2020, https://iem-student.org/2020/10/02/question-of-the-day-15/, date accessed: November 25, 2020

You may want to read these

Question Of The Day #14

question of the day
question of the day 14
40.1 - Pneumothorax 1

Which of the following is the most appropriate treatment for this patient’s condition?

Anticoagulation (Choice A) would be the proper treatment for pulmonary embolism, NSTEMI/STEMI, and other conditions. This patient is dyspneic and hypoxemic on the exam, but his chest X-ray offers an alternative explanation for his symptoms. IV antibiotics (Choice D) would be helpful for pneumonia and COPD exacerbation, both of which are possible in this patient, but his chest X-ray offers an alternative explanation for his symptoms. Needle decompression of the left chest (Choice B) would be the appropriate initial treatment for a left-sided “tension” pneumothorax. This patient does have a large left-sided pneumothorax, but the X-ray lacks tracheal deviation, mediastinal shift, and left hemidiaphragm flattening, which can be attributed to tension pneumothorax. Most importantly, the patient lacks the hemodynamic instability that defines tension physiology (i.e. hypotension and tachycardia). In addition, the diagnosis and treatment of tension pneumothorax should be made clinically prior to chest radiography. Signs of hemodynamic instability along with tracheal deviation, absent unilateral lung sounds, and a history of trauma all support a diagnosis of tension pneumothorax. The treatment of a tension pneumothorax requires prompt recognition, needle decompression at the 3rd intercostal space at the midclavicular line, and a tube thoracostomy at the 4-5th intercostal space the anterior axillary line. The recommended needle decompression location is recently shifted to 4-5th intercostal space at the mid-anterior axillary line because the studies showed lower success rates in anterior – mid clavicular approach in adults. This patient has a spontaneous left-sided pneumothorax, not a tension pneumothorax. This is likely secondary to his coughing episodes and severe COPD. The treatment for this would be supplemental oxygen and the placement of a small-bore chest tube (i.e. “pig tail) in the left chest. Correct Answer: C. 

References

Smith LM, Mahler SA. Chest Pain. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill; Accessed August 17, 2020. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=219641169

Nickson, C. (2019) Pneumothorax CCC. Life in the Fastlane. Accessed August 17, 2020. https://litfl.com/pneumothorax-ccc/

Cite this article as: Joseph Ciano, USA, "Question Of The Day #14," in International Emergency Medicine Education Project, September 25, 2020, https://iem-student.org/2020/09/25/question-of-the-day-14/, date accessed: November 25, 2020

Question Of The Day #13

question of the day
qod13

Which of the following is the most appropriate next step in management for this patient’s condition?

This patient presents to the emergency department after an atypical, brief episode of chest pain. The list of potential diagnoses that may have caused the pain episodes is extensive. The focus of the Emergency Medicine practitioner should not be to determine the diagnosis per say, but rather to be to identify the presence of any life-threatening conditions (i.e. Myocardial infarction, Aortic dissection, Esophageal Rupture, Pulmonary embolism, Tension pneumothorax, Cardiac tamponade, etc.). Many of these serious diagnoses can be evaluated with a detailed history, physical exam, and basic imaging and lab work if needed. Many risk stratification tools have been developed to evaluate the likelihood a patient has chest pain due to Acute Coronary Syndrome. One well-supported tool with international validation is the HEART score tool. The HEART score categorizes a patient as low (0-3), moderate (4-6), or high risk (7-10) for a Major Adverse Cardiac Event (MACE) based on the patient’s history, EKG, age, risk factors, and troponin level. The below chart from Wieters et al. (2020) outlines the HEART score categories and how to make clinical decisions based on a patient’s score.

HEART score for cardiac risk assessment of major adverse cardiac event (MACE).

CategoryScoreExplanationRisk Features
HistoryHigh-risk features
• Middle- or left-sided chest pain
• Heavy chest pain
• Diaphoresis
• Radiation
• Nausea and vomiting
• Exertional
• Relief of symptoms by sublingual nitrates

Low-risk features
• Well localized
• Sharp pain
• Non-exertional
• No diaphoresis
• No nausea and vomiting
Slightly Suspicious 0Mostly low-risk features
Moderately Suspicious+1Mixture of high-risk and low-risk features
Highly Suspicious+2Mostly high-risk features
ECG
Normal0Completely Normal
Non-specific Repolarization Disturbance+1Non-specific repolarization disturbance• Repolarization abnormalities
• Non-specific T wave changes
• Non-specific ST wave depression or elevation
• Bundle branch blocks
• Pacemaker rhythms
• Left ventricular hypertrophy
• Early repolarization
• Digoxin effect
Significant ST Depression+2Significant ST depression• Ischemic ST-segment depression
• New ischemic T wave inversions
Age
<450
45-64+1
≥ 65+2
Risk Factors• Obesity (Body-Mass Index ≥ 30)
• Current or recent (≤ 90 days)smoker
• Currently treated diabetes mellitus
• Family history of coroner artery disease (1st degree relative < 55 year old)
• Hypercholesterolemia

OR

Any history of atherosclerotic disease earn 2 points:
• Know Coroner artery Disease: Prior myocardial infarctions, percutan coronary intervention (PCI) or coronary artery bypass graft
• Prior stroke or transient ischemic attack
• Peripheral arterial disease
No known risk factors0
1-2 risk factors+1
≥ 3 risk factors or history of atherosclerotic disease+2
Initial Troponin
≤ normal limit0
1-3 x normal limit+1
> 3x normal limit+2

Score 0–3 = 2.5 % MACE over next 6 wk: Discharge home
Score 4–6 = 22.3% MACE over next 6 wk: Admit for observation
Score 7–10 = 72.7% MACE over next 6 wk: Admit with early invasive strategies

The patient’s HEART score in this question would be 2 (1 point for age and 1 point for hypertension as a risk factor). This categorizes the patient as low risk for a MACE over the next six weeks. The appropriate course of action for this patient would be discharge home with prompt outpatient follow-up (Choice B). Admission for cardiac testing (Choice D) would be warranted for a moderate-high risk HEART score. Prescribing a benzodiazepine (Choice C) would not be warranted as this patient is asymptomatic and the pain episode is vague and atypical. Benzodiazepines are sometimes useful in patients with chest pain due to anxiety. Cardiology consultation (Choice A) would not be warranted as the patient has a low HEART score, is currently asymptomatic with normal imaging, blood work and troponin, and a normal EKG. Correct Answer: B 

References

Smith LM, Mahler SA. Chest Pain. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill; Accessed August 17, 2020. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=219641169

Wieters J, McDonough J, Catral J. Chest Pain. In: Stone C, Humphries RL. eds. CURRENT Diagnosis & Treatment: Emergency Medicine, 8e. McGraw-Hill; Accessed August 17, 2020. https://accessmedicine.mhmedical.com/content.aspx?bookid=2172&sectionid=165059275

Cite this article as: Joseph Ciano, USA, "Question Of The Day #13," in International Emergency Medicine Education Project, September 18, 2020, https://iem-student.org/2020/09/18/question-of-the-day-13/, date accessed: November 25, 2020

Drop the Beat! – Adenosine in SVT

Drop the Beat! – Adenosine in SVT

Supraventricular tachycardia (SVT) is defined as a dysrhythmia that originates proximal to (or ‘above’) the atrioventricular (AV) node of the heart. It commonly manifests as a regular, narrow complex (QRS interval < 120ms) tachycardia in affected patients. It is most frequently attributable to re-entrant electrical conduction through accessory pathways in the heart, with typical Electrocardiogram (ECG) findings depicting ventricular rates of 150 to 250 beats/min without the preceding P wave usually seen in sinus tachycardias. [1,2]

In the stable adult patient presenting with SVT, where no ‘red flags’ such as shock, altered mental state, ischemic chest pain or hypotension are present, management typically begins with an attempt to convert the rhythm back to its baseline sinus state using vagal manoeuvres.[3] Vagal manoeuvres such as the carotid sinus massage and the Valsalva manoeuvre are effective first-line therapies, terminating approximately 25% of spontaneous SVTs,[4] with the newer, modified Valsalva manoeuvre showing even greater efficacy of 43% conversion.[5] When these fail or are otherwise not feasible to use in patients, management involves the administration of a drug called Adenosine.

The Evolution of Adenosine Use for SVT

In 1927, studies found that the injection of extracts from cardiac tissue into animals appeared to decrease heart rates and that this effect was attributable to an ‘adenine compound’.[6] This compound was later identified as Adenosine, comprised of the purine-based nucleobase Adenine attached to a ribose sugar. Fifty years after its initial discovery, Adenosine began to emerge as a treatment for stabilizing SVTs and has remained a mainstay in its management ever since.[7]

Current guidelines recommend Adenosine for the management of SVT, usually administered through a peripheral intravenous (IV) access initially as a 6 mg bolus. Adenosine has an extremely short half-life (less than 10 seconds) and is therefore rapidly metabolized soon after it enters the body.[8] Therefore, IV dosage is commonly followed by a 20 mL rapid saline flush to facilitate the drug’s transport to cardiac tissue where it can act before being broken down into inactive metabolites. If the 6mg dose does not convert the SVT back to sinus rhythm, subsequent doses are given at 12 mg, also followed by 20-mL saline for rapid infusion.

Pro-Tip: Single syringe technique

Before we dive into the concept of the single syringe method of administering Adenosine, take a look at the segment above. How would you give 6 mg of Adenosine through an IV site, making sure a total of 20 mL saline follows right after, in enough time to make sure you don’t waste that precious 10-second half-life of Adenosine? In many places, one of the two methods are used to make this happen:

  1. Use an IV line to push Adenosine > remove syringe > push 10 mL saline using a pre-filled syringe > remove syringe > push 10mL saline using a second pre-filled syringe.
  2. Fancier places use what’s known as a stopcock, a device usually with 3 ports attached to the IV site. Adenosine syringe is attached to one port and a 10 mL saline flush is attached at a separate port. The process looks something like this: Push adenosine through stopcock port > turn stopcock to open saline port’s access to IV site > push 10 mL saline flush > push an additional 10 mL saline using second syringe or remainder of a 20 mL prefilled syringe.

Now we all know that nurses are indistinguishable from ninjas at times when handling IV medication. However, even the most experienced practitioner is not immune to the occasional stumble when switching between the various syringes and swivels required in the methods above. In fact, a study in 2018 found that, in pediatric patients, adenosine given using the stopcock method delivered suboptimal doses.[9]

In an attempt to improve administration time, a potential work-around was proposed where adenosine could be combined with the flush solution in one 20 mL syringe and pushed altogether.[10] This potentially eliminates any time wasted changing syringes and manipulating stopcocks, but does it still work the same? Fortunately, a few studies have demonstrated the feasibility of the single syringe method, with non-inferior efficacy compared to standard methods of drug administration.[11,12]

Caveats: Coffee Conundrums

Let’s talk a bit about dosage. We mentioned above that guidelines recommend starting at 6 mg and moving to 12 mg for subsequent dosages. These dosages assume uninhibited action of adenosine at its receptors which, unfortunately, may not always be the case in patients. What would inhibit adenosine’s activity, I hear you ask? You’ll want to put down that Caramel Macchiato because the answer (pause for dramatic effect) … is coffee – caffeine to be exact.

Caffeine is known to work by antagonizing adenosine receptors, thereby decreasing adenosine’s biologic effect.[13] A component in many frequently consumed beverages, such as coffee, tea, energy drinks and sodas, and with a half-life of approximately 4-5 hours, caffeine is very likely to be present in the bloodstreams of many Emergency Department patients (and doctors). A 2010 multi-centre study in Australia found that recent ingestion of caffeine less than 4 hours prior to a 6 mg adenosine bolus significantly reduced its effectiveness in treating SVT. [14]

This makes it all the more important to not only include information on any known recent beverage consumption during history taking for patients presenting with SVT, but also to potentially increase dosage for patients with a confirmed or suspected recent ingestion of caffeine. In such cases, it would be reasonable to start at 12 mg adenosine as the first dose, followed by 18 mg subsequent dosages to manage SVT.[15]

A 2010 multi-centre study in Australia found that recent ingestion of caffeine less than 4 hours prior to a 6 mg adenosine bolus significantly reduced its effectiveness in treating SVT.

References and Further Reading

  1. Bibas, L., Levi, M., & Essebag, V. (2016). Diagnosis and management of supraventricular tachycardias. CMAJ : Canadian Medical Association journal = journal de l’Association medicale canadienne, 188(17-18), E466–E473. https://doi.org/10.1503/cmaj.160079
  2. Mahtani, A. U., & Nair, D. G. (2019). Supraventricular Tachycardia. The Medical clinics of North America, 103(5), 863–879. https://doi.org/10.1016/j.mcna.2019.05.007
  3. Advanced Cardiac Life Support Provider Manual, American Heart Association, Mesquite 2016
  4. Lim, S. H., Anantharaman, V., Teo, W. S., Goh, P. P., & Tan, A. (1998). Comparison of Treatment of Supraventricular Tachycardia by Valsalva Maneuver and Carotid Sinus Massage. Annals of emergency medicine, 31(1), 30–35.
  5. Appelboam, A., Reuben, A., Mann, C., Gagg, J., Ewings, P., Barton, A., Lobban, T., Dayer, M., Vickery, J., Benger, J., & REVERT trial collaborators (2015). Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. Lancet (London, England), 386(10005), 1747–1753. https://doi.org/10.1016/S0140-6736(15)61485-4
  6. Drury, A. N., & Szent-Györgyi, A. (1929). The physiological activity of adenine compounds with especial reference to their action upon the mammalian heart. The Journal of physiology, 68(3), 213–237. https://doi.org/10.1113/jphysiol.1929.sp002608
  7. Delacrétaz E. (2006). Clinical practice. Supraventricular tachycardia. The New England journal of medicine, 354(10), 1039–1051. https://doi.org/10.1056/NEJMcp051145
  8. Kazemzadeh-Narbat, M., Annabi, N., Tamayol, A., Oklu, R., Ghanem, A., & Khademhosseini, A. (2015). Adenosine-associated delivery systems. Journal of drug targeting, 23(7-8), 580–596. https://doi.org/10.3109/1061186X.2015.1058803
  9. Weberding, N. T., Saladino, R. A., Minnigh, M. B., Oberly, P. J., Tudorascu, D. L., Poloyac, S. M., & Manole, M. D. (2018). Adenosine Administration With a Stopcock Technique Delivers Lower-Than-Intended Drug Doses. Annals of emergency medicine, 71(2), 220–224. https://doi.org/10.1016/j.annemergmed.2017.09.002
  10. Hayes, B.D. (2019). ‘Trick of the Trade: Combine Adenosine with the Flush’. Academic Life in Emergency Medicine Blog Post https://www.aliem.com/trick-of-trade-combine-adenosine-single-syringe/
  11. Choi, S.C., Yoon, S.K., Kim, G.W., Hur, J.M., Baek, K.W., & Jung, Y.S. (2003). A Convenient Method of Adenosine Administration for Paroxysmal Supraventricular Tachycardia. Journal of the Korean society of emergency medicine, 14, 224-227.
  12. McDowell, M., Mokszycki, R., Greenberg, A., Hormese, M., Lomotan, N., & Lyons, N. (2020). Single-syringe Administration of Diluted Adenosine. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 27(1), 61–63. https://doi.org/10.1111/acem.13879
  13. Ribeiro, J. A., & Sebastião, A. M. (2010). Caffeine and adenosine. Journal of Alzheimer’s disease : JAD, 20 Suppl 1, S3–S15. https://doi.org/10.3233/JAD-2010-1379
  14. Cabalag, M. S., Taylor, D. M., Knott, J. C., Buntine, P., Smit, D., & Meyer, A. (2010). Recent caffeine ingestion reduces adenosine efficacy in the treatment of paroxysmal supraventricular tachycardia. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 17(1), 44–49. https://doi.org/10.1111/j.1553-2712.2009.00616.x
  15. Hayes, B.D. (2012). ‘Is the 6-12-12 adenosine approach always correct?’ Academic Life in Emergency Medicine Blog Post https://www.aliem.com/is-6-12-12-adenosine-approach-always/
Cite this article as: Mohammad Anzal Rehman, UAE, "Drop the Beat! – Adenosine in SVT," in International Emergency Medicine Education Project, September 14, 2020, https://iem-student.org/2020/09/14/adenosine-in-svt/, date accessed: November 25, 2020

Question Of The Day #12

question of the day

Which of the following medications should be avoided to prevent worsening of this patient’s condition?

This elderly female patient presents with chest pain described as post-prandial burning, radiating to the shoulders, and with associated nausea and diaphoresis. Burning chest pain after eating supports diagnoses, such as peptic ulcer disease, gastritis, gastroesophageal reflux, or biliary disease. However, chest pain that radiates to both shoulders (2.58 likelihood ratio) or has associated diaphoresis (1.50 likelihood ratio) should be very concerning for acute myocardial infarction (Smith & Mahler, 2020). Associated symptoms that should raise concern for acute coronary syndrome are any radiation of the chest pain, pain worsened with exertion, associated nausea or vomiting, pain described as pressure or squeezing, pain with associated diaphoresis, and pain described as feeling similar to prior ischemic events. This patient’s EKG demonstrates an inferior ST-segment elevation myocardial infarction (STEMI). This is indicated by two or more inferior EKG leads (II, III, and aVF) showing ST-segment elevation greater than 1 mm and reciprocal ischemic changes indicated in lateral leads (I, aVL). Aspirin (Choice A) should be given to all patients with high suspicion for ACS, assuming there are no contraindications. This patient has a confirmed STEMI on her EKG and should receive Aspirin for its antiplatelet effects. Ibuprofen (Choice B) may help the patient’s pain, but likely would not acutely worsen the patient’s clinical condition. Antacids (Choice C) are relatively benign medications, and they would be unlikely to worsen the patient’s clinical condition. Nitroglycerin (Choice D) is often given in patients with anginal chest pain for pain relief. In many inferior STEMIs, nitroglycerin can cause a dangerous drop in blood pressure and should be avoided. These patients may have infarction of the right ventricle, which makes these patients sensitive to nitrates and prone to precipitous drops in blood pressure. IV fluids are the preferred initial therapy in the setting of hypotension. About 40% of patients with an inferior STEMI have concurrent right ventricular infarction. About 80% of inferior STEMIs are caused by occlusions in the right coronary artery (RCA) and about 18% are from an occlusion in the left circumflex artery (LCx). Occluded vessels in both territories can cause right ventricular infarction. Correct Answer: D  

References

Smith LM, Mahler SA. Chest Pain. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill; Accessed August 17, 2020. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=219641169

Burns, E. (2019) Inferior STEMI. Life in the Fast Lane. Accessed August 17, 2020. https://litfl.com/inferior-stemi-ecg-library/

Cite this article as: Joseph Ciano, USA, "Question Of The Day #12," in International Emergency Medicine Education Project, September 11, 2020, https://iem-student.org/2020/09/11/question-of-the-day-12/, date accessed: November 25, 2020

Question Of The Day #10

question of the day
qod10 palpitation

Which of the following is the most appropriate next step in management for this patient’s condition?

This patient has a narrow-complex tachycardia with a regular rhythm. A narrow QRS complex is defined as a QRS interval less than 120msec. This is a normal finding. The differential diagnoses for regular narrow complex tachycardia include sinus tachycardia, atrial tachycardia, atrial flutter, and supraventricular tachycardia (“SVT”). SVTs are typically associated with narrow QRS complexes, unless there is a concurrent bundle branch block, other aberrant conduction, or the existence of electrical accessory pathways as in Wolff Parkinson White (WPW) syndrome. The heart rate of an SVT can vary from 140-280 beats/min. Intravenous Adenosine (Choice A) is a hallmark of SVT treatment, however, Adenosine is given after vagal maneuvers have been attempted and have failed. Synchronized cardioversion (Choice B) is a last-ditch effort treatment in a patient with SVT. Vagal maneuvers and medications are attempted prior to using cardioversion. However, if the patient is hypotensive, cardioversion should be employed. Intravenous Amiodarone (Choice C), beta-blockers, calcium channel blockers, or other antiarrhythmics can be used to terminate SVTs if vagal maneuvers and adenosine are not effective. Vagal maneuvers (Choice D), such as the Valsalva maneuver (“bearing down”) or carotid massage, are the initial treatment for SVTs. Correct Answer: D 

References

Burns, E. (2019, March 30). Supraventricular Tachycardia (SVT). Life in the Fast Lane. https://litfl.com/supraventricular-tachycardia-svt-ecg-library/

Nickson, C. (2019, March 24). Narrow Complex Tachycardia. Life in the Fast Lane. https://litfl.com/narrow-complex-tachycardia/

Cite this article as: Joseph Ciano, USA, "Question Of The Day #10," in International Emergency Medicine Education Project, August 28, 2020, https://iem-student.org/2020/08/28/question-of-the-day-10/, date accessed: November 25, 2020