Question Of The Day #21

question of the day

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.


Cite this article as: Joseph Ciano, USA, "Question Of The Day #21," in International Emergency Medicine Education Project, November 13, 2020,, date accessed: November 24, 2020

Question Of The Day #20

question of the day
608 - Figure3 - pericardial effusion - ECG

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

This patient’s EKG demonstrates alternating amplitudes of QRS complexes, a phenomenon known as electrical alternans. This is caused by the heart swinging back and forth within a large pericardial effusion. The patient is tachycardic and borderline hypotensive, which should raise concern over impending cardiac tamponade. The next best investigation to definitively diagnose a large pericardial effusion with possible tamponade would be a cardiac sonogram (Choice B). This investigation could also guide treatment with pericardiocentesis in the event of hemodynamic decompensation and the development of obstructive shock. Other EKG signs of a large pericardial effusion are diffusely low QRS voltages and sinus tachycardia. Chest radiography (Choice C) may show an enlarged cardiac silhouette in this case and evaluate for alternative diagnoses (i.e. pneumothorax, pleural effusions, pneumonia, atelectasis), however, cardiac echocardiography is the best next investigation. CT pulmonary angiography (Choice D) would demonstrate the presence of a pericardial effusion along with differences in cardiac chamber size indicative of tamponade. Still, bedside cardiac sonogram is a faster test that prevents a delay in diagnosis. Sending a potentially unstable patient for a CT scan may also be dangerous. Arterial blood gas testing (Choice A) has no role in diagnosing pericardial effusion or cardiac tamponade. Correct Answer: B


Cite this article as: Joseph Ciano, USA, "Question Of The Day #20," in International Emergency Medicine Education Project, November 6, 2020,, date accessed: November 24, 2020

From Missed Hemodialysis to Multiple Arrhythmias

From Missed Hemodialysis to Multiple Arrhythmias

Case Presentation

A 78-year-old male, known case of Chronic Kidney Disease on maintenance hemodialysis, presented to the Emergency Department with dizziness and lethargy complaints about 2 days. He had missed his last hemodialysis session due to personal reasons. We could not elicit any further history details as was significantly dyspneic (no bystanders with him at the time of presentation). Hence, the patient was received in Bay 1 for immediate resuscitative measures. The patient was afebrile, conscious, and well oriented, but unable to communicate because of severe dyspnea.


HR – 142 beats/min
BP – not recordable
RR – 36 breaths/min
SpO2 – poor tracing, intermittently showed 98% on room air (15 LO2 via Non Rebreathing Mask was initiated nevertheless)


ECG on presentation
Monomorphic ventricular tachycardia

He was immediately connected to a defibrillator in anticipation of possible synchronized cardioversion. Simultaneously, the cause of the possible rhythm was being evaluated for and a thorough examination was carried out. On examination, his lung fields were clear. His left arm AV Fistula had a feeble thrill on palpation.

In suspicion of hyperkalemia as the cause of VT, patient was immediately started on potassium reduction measures while the point of care ABG report was awaited. He was treated with salbutamol nebulization 10mg, sodium bicarbonate 50 ml IV and 10% calcium gluconate 10ml IV. In view of hemodynamic instability, he was also started on intravenous noradrenaline infusion.

ABG Findings

pH – 7.010, pCO2 – 20.8 mmHg, pO2 – 125 mmHg, HCO3 – 7 mmol/L, Na – 126 mmol/L, K – 9.6 mmol/L

As hyperkalemia was confirmed, the patient was also given 200 ml of 25% dextrose with 12 units of Rapid-acting insulin IV. With the above measures, the patient’s cardiac rhythm came to a sine wave pattern. 

He was later taken up for emergency hemodialysis (HD) – Sustained Low Efficacy Dialysis (SLED) in the ICU, using a low potassium dialysate. Since his AV fistula was non-functioning, HD was done after placement of a femoral dialysis catheter. 2 hours into HD, the patient’s cardiac monitor showed a normal sinus rhythm. His hemodynamic status significantly improved. Noradrenaline infusion was gradually tapered and stopped by the end of the HD session, and repeat blood gas analysis and serum electrolytes showed improvement of all parameters. 

after hemodialysis

The patient was discharged 2 days later, after another session of hemodialysis (through AV fistula) and a detailed cardiology evaluation (ECHO – LVH, normal EF).

For the Inquisitive Minds

  1. The patient underwent a detailed POCUS evaluation, both in the ER and ICU. What findings do you expect to find on the RUSH examination for this patient?
  2. His previous ECHO report (done 1 month ago) mentioned left ventricular hypertrophy and normal ejection fraction. So what would be the reason behind the POCUS findings? Is it reversible?
  3. Why was the AV fistula non-functioning at the time of presentation? When would it have started to function again?
  4. Despite not having hypoxia, this patient was given supplemental oxygen. Did he really require it, and if so, what was the rationale?
  5. What was the necessity for carrying out SLED for this patient?
  6. Why was this patient not immediately cardioverted in the ER?
  7. If this patient had gone into cardiac arrest, what drugs would you have given for management of hyperkalemia?
  8. How differently would you have managed this patient?

Please give your answers and comments into "leave a reply" area below.

Cite this article as: Gayatri Lekshmi Madhavan, India, "From Missed Hemodialysis to Multiple Arrhythmias," in International Emergency Medicine Education Project, November 2, 2020,, date accessed: November 24, 2020
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Question Of The Day #19

question of the day
52 - Perforated Viscus

Which of the following is the most likely cause of the patient’s condition?

All patients who present to the emergency department with chest pain should be evaluated for the top life-threatening conditions causing chest pain. Some of these include myocardial infarction, pulmonary embolism, esophageal rupture, tension pneumothorax, cardiac tamponade, and aortic dissection. Many of these diagnoses can be ruled-out or deemed less likely with a detailed history, physical exam, EKG, and sometimes imaging and blood testing. This patient presents with vague, burning chest pain, nausea, and tachycardia on exam. Pulmonary embolism (Choice A) is hinted by the patient’s tachycardia, but the patient has no tachypnea or risk factors mentioned for PE. Additionally, the chest X-ray findings demonstrate an abnormality that can explain the patient’s symptoms. Pancreatitis (Choice B) and Gastroesophageal reflux disorder (Choice D) are also possible diagnoses, especially with the location and description of the patient’s pain. However, Chest X-ray imaging offers an explanation for the patient’s symptoms. The patient’s Chest X-ray demonstrates the presence of pneumoperitoneum. In the presence of NSAID use, this radiological finding raises concern over a perforated viscus from advanced peptic ulcer disease (Choice C). Peptic ulcer disease (PUD) is most commonly caused by Helicobacter pylori infection, but NSAIDs, iron supplements, alcohol, cocaine, corrosive substance ingestions, and local infections can cause PUD. PUD is a clinical diagnosis which can be confirmed visually via endoscopy. The treatment for PUD includes initiation of a proton pump inhibitor (H2-receptor blockers are 2nd line), avoiding the inciting agent, and H.pylori antibiotic regimens in confirmed H.pylori cases. The treatment for a perforated peptic ulcer with pneumoperitoneum is IV fluids, IV antibiotics, Nasogastric tube placement, and surgical consultation for repair.


Cite this article as: Joseph Ciano, USA, "Question Of The Day #19," in International Emergency Medicine Education Project, October 30, 2020,, date accessed: November 24, 2020

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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?


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,, date accessed: November 24, 2020

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

Question Of The Day #18

question of the day
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 


Cite this article as: Joseph Ciano, USA, "Question Of The Day #18," in International Emergency Medicine Education Project, October 23, 2020,, date accessed: November 24, 2020

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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
Malignancy w/ Treatment within 6 mo, or palliative+1
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 


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.

Nickson, C. (2019). Pulmonary Embolism. Life in the Fastlane. Accessed on August 17, 2020.

Cite this article as: Joseph Ciano, USA, "Question Of The Day #15," in International Emergency Medicine Education Project, October 2, 2020,, date accessed: November 24, 2020

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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. 


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.

Nickson, C. (2019) Pneumothorax CCC. Life in the Fastlane. Accessed August 17, 2020.

Cite this article as: Joseph Ciano, USA, "Question Of The Day #14," in International Emergency Medicine Education Project, September 25, 2020,, date accessed: November 24, 2020

Question Of The Day #13

question of the day

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
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
≥ 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


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 


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.

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.

Cite this article as: Joseph Ciano, USA, "Question Of The Day #13," in International Emergency Medicine Education Project, September 18, 2020,, date accessed: November 24, 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.
  2. Mahtani, A. U., & Nair, D. G. (2019). Supraventricular Tachycardia. The Medical clinics of North America, 103(5), 863–879.
  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.
  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.
  7. Delacrétaz E. (2006). Clinical practice. Supraventricular tachycardia. The New England journal of medicine, 354(10), 1039–1051.
  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.
  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.
  10. Hayes, B.D. (2019). ‘Trick of the Trade: Combine Adenosine with the Flush’. Academic Life in Emergency Medicine Blog Post
  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.
  13. Ribeiro, J. A., & Sebastião, A. M. (2010). Caffeine and adenosine. Journal of Alzheimer’s disease : JAD, 20 Suppl 1, S3–S15.
  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.
  15. Hayes, B.D. (2012). ‘Is the 6-12-12 adenosine approach always correct?’ Academic Life in Emergency Medicine Blog Post
Cite this article as: Mohammad Anzal Rehman, UAE, "Drop the Beat! – Adenosine in SVT," in International Emergency Medicine Education Project, September 14, 2020,, date accessed: November 24, 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  


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.

Burns, E. (2019) Inferior STEMI. Life in the Fast Lane. Accessed August 17, 2020.

Cite this article as: Joseph Ciano, USA, "Question Of The Day #12," in International Emergency Medicine Education Project, September 11, 2020,, date accessed: November 24, 2020

Hypokalemic Periodic Paralysis in the ED

Hypokalemic Periodic Paralysis in the ED

Case Presentation

A middle-aged man with a two days history of weakness in his legs. The patient works as a construction worker and is used to conducting heavy physical activity.

After a thorough history and examination, the weakness was reported in the lower extremities with a power of 2/5, whereas the power in upper extremities was 4.5/5, Achilles tendon reflex was reduced, plantar response and other reflexes were intact, with normal sensation. Rest of the examination is unremarkable.

The vitals are within normal ranges, Blood investigations include – Urea and electrolytes, liver and renal function, full blood count, thyroid function tests, creatine kinase, urine myoglobin, vitamin B12 and folic acid levels.

Potassium level was 1.7 mEq/L (normal 3.5-5.5), and all other parameters were within normal ranges.

The ECG showed inverted T waves and the presence of U waves. An Example of an ECG:

Hypokalemic periodic paralysis is a rare disorder that may be hereditary as the primary cause, or secondary due to thyroid disease, strenuous physical activity, a carbohydrate-rich meal and toxins. The patients are mostly of Asian origin.

The most common presentation is of symmetrical weakness in lower limbs, with a low potassium level and ECG changes of hypokalemia. The patients may have a history of similar weaknesses which may be several years old. An attack may be triggered by infections, stress, exercise and other stress-related factors.

The word ‘weakness’, can lead to physicians thinking about stroke, neurological deficits and other life-threatening illnesses such as spinal cord injuries associated with high morbidity and mortality which need to be ruled out in the ED.

In this case, history and examination are vital. Weakness in other parts of the body, a thorough neurological examination are important aspects.

Patients are monitored and treated with potassium supplements (oral/Intravenous) until the levels normalize. ECG monitoring is essential, as cardiac function may be affected. 

The patient should be examined to assess the strength and should be referred for further evaluation and to confirm the diagnosis.

The differential diagnosis for weakness in lower limb include :

  1. Spinal cord disease (
  2. Guillain barre syndrome
  3. Toxic myositis
  4. Trauma
  5. Neuropathy
  6. Spinal cord tumour


Cite this article as: Sumaiya Hafiz, UAE, "Hypokalemic Periodic Paralysis in the ED," in International Emergency Medicine Education Project, September 7, 2020,, date accessed: November 24, 2020