Apple Podcasts , Spotify, Listen Here
Panscans, or a combination of head to pelvis CT scans, have been used in patients following significant trauma. Recent attention has shifted to the utility of routine CT scans following cardiac arrest. This is based on (1) identification of potential causes of cardiac arrest (2) identification of complications of resuscitation. In this episode, we cover an article by Branch et al in Academic Emergency Medicine.
We are at #SMACC in Sydney, Australia, thanks to the Rosh Review, delivering updates from the conference to your earbuds.
Mechanical CPR vs Manual CPR – Ken Milne vs Salim Rezaie
Massive GI Bleed and Balloon Tamponade – Dr. Sara Gray
Blakemore, Linton, and Minnesota Tube Review Video
Advocacy in Emergency Medicine – Esther Choo and Hugh Montgomery
Dr. Choo spoke about how she became an advocate and helped start TIMES UP HEALTHCARE. Check out her NEJM perspective article.
Hugh Montgomery spoke on ways to motivate individuals to change behavior by appealing to emotional aspects.
We co-hosted (with John Vassiliadis) the #smacc EM Updates half-day conference. We had amazing speakers. Salim Rezaie spoke on TXA for Everything, Ken Milne spoke on hot papers from 2018, and we learned about when ultrasound may be helpful in pediatric lumbar punctures. In addition, Jeremy spoke on what is usual care in sepsis and Lauren spoke on pulmonary embolism: the next generation. In this short podcast we highlight some of our other talks.
Aidan Baron (@Aidan_Baron) on Prehospital Updates in Cardiac Arrest
This talk focused on focusing on things that are most likely to make a difference in OHCA (bystander CPR and defibrillation) rather than on fun interventions like intubation and adrenaline (epinephrine). Aidan suggests that the future debates and questions in OHCA will be largely philosophical – what outcomes do we care about: neuro intact survival or ROSC or survival?
Low-Risk Chest Pain and the HEART Score by Barbra Backus
Modified Heart Score (redefining the T or troponin based on newer assays) results in a NPV of 99.8% and classifies 48% of patients as low-risk.
Clinically Relevant Adverse Cardiac Events (CRACE) is way less common than major adverse cardiac events (MACE). HEART score of ≤3 ? CRACE is 0.05%
Hot Literature in 2019
Lemkes JS, Janssens GN, van der Hoeven NW, et al. Coronary Angiography after Cardiac Arrest without ST-Segment Elevation. N Engl J Med. 2019;NEJMoa1816897
Pluymaekers NAHA, Dudink EAMP, Luermans JGLM, et al. Early or Delayed Cardioversion in Recent-Onset Atrial Fibrillation. N Engl J Med .2019;NEJMoa1900353.
Special thanks to the Rosh Review for supporting our trip to SMACC!
We have previously podcasted on tachyarrythmias (Episode 34 Tachyarrhythmias), but in this episode, we focus specifically on the treatment of supraventricular tachycardia (SVT), specifically paroxysmal SVT.
Adenosine and calcium channel blockers are both commonly used in the treatment of SVT; however, practice often varies by region. Advantages to adenosine are the short half-life but this comes with a trade-off of patients experiencing terrifying feelings as they have a sinus pause. Calcium channel blockers have the advantage of not causing those side effects and may prevent recurrence, but patients may infrequently experience hypotension [3,4]. Adenosine and calcium channel blockers are both contra-indicated in pre-excitation syndromes as they may precipitate ventricular fibrillation. A case series is often cited as a reason to not give calcium channel blockers in SVT; however, in these cases 4 of the 5 patients were treated for atrial fibrillation with rapid ventricular response NOT SVT and all patients had signs of preexcitation on their ECG in which use of nodal blockers are discouraged [5]. Both adenosine and calcium channel blockers are recommended by the AHA [1]. In fact, the AHA recommendation for calcium channel blockers in SVT is higher than that for epinephrine in out of hospital cardiac arrest (which is a Class IIb recommendation).
Personally, we like calcium channel blockers for the treatment of stable SVT in patients who do not have signs of pre-excitation.
A 2-month-old male infant presents with rapid heart rate from the pediatrician’s office. The baby’s blood pressure is normal for age and he appears interactive with mom. ECG confirms your suspicion of supraventricular tachycardia. What is the mechanism of action of the medication of choice?
A. Blocks accessory pathway re-entry
B. Decreases conduction through the accessory pathway
C. Decreases conduction through the atrioventricular node and blocks atrioventricular nodal re-entry
D. Increases conduction through the atrioventricular node and blocks atrioventricular nodal re-entry
[accordion]
[toggle title=”Answer” state=”closed”]
C. Adenosine is the pharmacologic treatment of choice for supraventricular tachycardia (SVT). It is a purine nucleoside that decreases the rate of conduction through the atrioventricular (AV) node and blocks AV nodal re-entry. It works directly on adenosine receptors at the AV node. By decreasing the rate of conduction, adenosine effectively slows the anterograde entry of SVT. By blocking AV nodal re-entry, it effectively stops retrograde conduction through the AV node. Thus, adenosine works well for SVT with and without accessory pathways. Adenosine is a very short acting medication and is metabolized quickly, so it should be given as close to the heart as possible. It should be administered through a large gauge peripheral IV, with a flush of 5 to 10 mL of normal saline, traditionally using a 3-way stopcock. SVT is the most common dysrhythmia in childhood. Often, children with SVT are relatively stable. Heart rates for infants are generally over 220 beats per minute and over 180 beats per minute in young children under 2 years old. In children who have normal mentation and stable blood pressures, IV access should be obtained and vagal maneuvers may be attempted. If a child is unstable, synchronized cardioversion at 0.5-1 J/kg should be performed as soon as possible. Cardiology should be consulted for further management, including accessory pathway ablation in many cases.
Adenosine does not block accessory pathway re-entry (A). Adenosine also does not slow forward conduction of the accessory pathway (B). It only works at the AV node and blocks AV re-entry. Adenosine is effective only at the adenosine receptors on the AV node. Adenosine does not increase conduction through the atrioventricular node (D) but rather decreases conduction at the AV node.
/toggle]
[/accordion]
References:
The US Food and Drug Administration (FDA) recently released another warning for fluoroquinolones, this time regarding aortic dissection and aneurysm.
Much of the evidence behind this warning comes from these studies, released in 2015 and 2018 [1-3].
We also review the ACEP Clinical Policy on thoracic aortic dissections [4].
Check out Figure 1 cases on aortic dissection (free educational app for healthcare providers)
A 75-year-old man presents to the emergency department with acute onset of chest pain that radiates to his upper back. Which of the following features would help support a diagnosis of an aortic dissection?
A. A difference of 24 mm Hg in the systolic blood pressures between the upper extremities
B. An increase in heart rate of 120 beats per minute with standing
C. Auscultation of a carotid bruit
D. Chest pain that worsens with inspiration and improves with expiration
[accordion]
[toggle title=”Answer” state=”closed”]
A. An aortic dissection is relatively rare, but it can be life-threatening, so early diagnosis and intervention are critical. They occur more commonly in men aged 60 to 80 years old. Dissections occur secondary to tears in the aortic intima. They can develop due to trauma or degeneration of the aortic media. This deficit in the aorta causes blood to pass into the aortic media, which separates the intima from the surrounding media or adventia. A false lumen then results. Death can occur if the the dissection continues into the aortic valve causing severe aortic regurgitation or if the dissection ruptures into the pericardium causing cardiac tamponade. Other factors that increase mortality include obstruction of the abdominal aortic branch vessels causing end-organ failure or obstruction of the coronary artery causing myocardial infarction. Aortic dissections may be classified as acute or chronic. The acute phase is defined as the first two weeks, and during this time period, the risk of complications or aortic rupture is much higher compared to the chronic phase. Patients will commonly complain of symptoms in the early morning hours as this may be the time of day when the blood pressure is elevated. Chest or back pain is the most common presenting symptom. Patients with a prior history of diabetes or an aortic aneurysm may present with heart failure, syncope, or stroke symptoms. The pain associated with an aortic dissection usually begins abruptly and is severe and sharp in nature with radiation to the back. Weak pulses may occur secondary to impaired blood flow to the peripheral vessels. Often, patients may maintain a variation of over 20 mm Hg in systolic blood pressure between the arms. If the dissection involves the aortic valve, a diastolic murmur associated with aortic regurgitation may be appreciated at the right sternal border. Hypertension is more common in patients with descending aortic dissection compared to hypotension, which is a more classic presentation of ascending aortic dissections. An increase in heart rate of 120 beats per minute with standing (B) would likely be associated with postural orthostatic tachycardia syndrome (POTS). Tachycardia may occur as a compensatory mechanism to the hypotension associated with a dissection but it would not be impacted by position changes. Postural orthostatic tachycardia syndrome tends to be more common in teenage girls and will present with anxiety, palpitations, or dizziness. The auscultation of a carotid bruit (C) would classically correlate with carotid artery disease and occurs secondary to turbulent blood flow. It is not commonly associated with an aortic dissection, however, it can correlate with an increased risk of stroke. Chest pain that worsens with inspiration and improves with expiration (D) often correlates with a pulmonary embolism. This type of pain is referred to as pleuritic. While this symptom is not sensitive or specific for an aortic dissection, any patient with chest pain should be thoroughly evaluated for potential cardiac pathology. [/toggle]
[/accordion]
We cover the clinical policy from the American College of Emergency Physicians – Clinical Policy: Critical Issues in the Evaluation and Management of Emergency Department Patients With Suspected Non–ST-Elevation Acute Coronary Syndromes
Check out our sponsor for this show, Figure 1, a free open access application for providers using images and cases.
Rosh Review Emergency Board Review Questions
An elderly man presents with 4 episodes of angina in the past 24 hours. His medical history includes diabetes and asthma. Based on initial testing, you diagnose non-ST-elevation myocardial infarction. You are waiting for the cardiac team to admit him to the critical care unit. In the interim, which of the following is the most appropriate medication to begin?
A. Atelplase
B. Clopidogrel
C. Digoxin
D. Metoprolol
[accordion]
[toggle title=”Answer” state=”closed”]
B. Non-ST-elevation myocardial infarction (NSTEMI) treatment begins with a basic anti-ischemic regimen consisting of oxygen, morphine, nitrates, and possibly beta-blockers and ACE-inhibitors. Antiplatelet medications are then considered. Choices include aspirin, clopidogrel, and prasugrel. NSTEMI treatment is rounded out with anticoagulants such as enoxaparin, bivalirudin, and fondaparinux. Based on risk stratification, definitive treatment may include medications-alone, angiography, percutaneous cardiac intervention or coronary artery bypass surgery. Clopidogrel acts by irreversibly inhibiting a platelet receptor that is needed for activation, thereby inhibiting platelet function. Thrombolytics (fibrinolytics), such as alteplase (A), reteplase and tenecteplase, are contraindicated in the treatment of NSTEMI, as they have shown worse outcomes with their use. Digoxin (C), a cardiac glycoside, is used in treating certain dysrhythmias and heart failure, not myocardial infarction. Beta-blockers such as metoprolol (D) carry a relative contraindication in patients with severe COPD, asthma, atrioventricular block, hypotension or bradycardia.
[/toggle]
[/accordion]
We cover the American College of Emergency Physicians clinical policy on Acute Venous Thromboembolic Disease (i.e. PE) [1]
Risk Stratification in Pulmonary Embolism
In the United States, the workup rate for PE is astonishingly high, with 1-2% of all ED patients receiving a CTPA for PE and a low yield (~5-10% of CTPAs are positive for PE). Thus, major medical societies such as ACEP and the American College of Physicians recommend the use of risk stratification tools [1,2]. For some reason, approximately 25% of patients who are low risk AND PERC negative still receive d-dimer or imaging for PE, despite the risk of PE being exceptionally low. To be clear, use of clinical decision tools are not mandatory and do not necessarily perform better than clinical gestalt [9]. These tools may serve as a “reality check” for some, reminding them that patients may be at lower risk of PE than they think
Rosh Review Emergency Board Review Questions
References:
Did you think blood pressure cuff readings were accurate? Guess again.https://t.co/vQc6BV2UGD @JACCJournals pic.twitter.com/f36ppi3Hrl
— Eric Topol (@EricTopol) July 25, 2017
Picone et al published a meta-analysis in the Journal of the American College of Cardiology discussing the accuracy of cuff blood pressures.
We cover core content on hypertension using the ACEP clinical policy on hypertension, Rosen’s (9th ed) Chapter 74 “Hypertension,” and Tintinalli (8th ed), Chapter 57 “Systemic Hypertension” Chapter 59 “Aortic Dissection and Related Aortic Syndromes” as guides. Check out this FOAM review of hypertension in the ED.
References:
We are in Berlin for #dasSMACC and have lots of pearls to share from the speakers at this amazing conference. Talks will be released for free on the SMACC podcast over the next year, but this podcast holds some pearls that we thought couldn’t wait.
Dr. Leanne Harnett on Pulmonary Embolism with Right Heart Thrombus (PE with RHT)
Drs. Reuben Strayer (@emupdates) and Scott Weingart (@emcrit) on Acute Hypertensive Pulmonary Edema
Dr. Michele Domico on Pediatric Cardiology Emergencies
Dr. Haney Mallemat (@CriticalCareNow) on Transesophageal Echocardiography (TEE) during Cardiac Arrest
For more on pulse checks, see this blog post.
References:
The Free Open Access Medical Education (FOAM)
In the United States, electrocardiograms (ECGs) performed in triage must often be signed by an attending emergency physician shortly after they are performed. This creates a significant number of interruptions which are not only inconvenient but also distracting for physicians taking care of patients. A recent study in Academic Emergency Medicine by Hughes and colleagues looks at the potential clinical relevance of having emergency physicians sign ECGs read “normal” by the computer software. FOAM reviews of this article can be found here:
The Core Content
Rosen’s Emergency Medicine (8th ed), Chapter 78 and the 2013 AHA Guidelines
ST Elevation MI (STEMI)
This is the time-dependent infarction with current goals to obtain reperfusion within 90 minutes (or 60 minutes at some hospitals).
However, there are more kinds of ischemia than just STEMI and many of these can be subtle. Close examination of even normal ECGs is necessary.
Rosh Review Emergency Board Review Questions
A 45-year-old man presents with chest pain. Which of the following features most strongly predicts acute coronary syndrome as the cause of his chest pain
A. History of diabetes mellitus, hypertension, and tobacco use
B. Pleuritic pain
C. Pressure-like pain
D. Radiation to the right arm
[accordion]
[toggle title=”Answer” state=”closed”]
D.
Chest pain is one of the most common presenting complaints to emergency departments. The causes of chest pain are varied and range from benign (e.g. muscle strain, costochondritis, pleurisy) to life-threatening (e.g. acute coronary syndrome, aortic dissection, pulmonary embolism). The emergency provider’s job is to carefully assess the patient with chest pain and rule out any life-threatening etiologies. As such, acute coronary syndrome must be considered on the differential of every patient presenting with chest pain. Acute coronary syndrome most commonly occurs when an atherosclerotic plaque is disrupted or eroded, resulting in platelet aggregation and thrombus formation at the site, resulting in diminished or absent flow within the affected vessel. Historical features are extremely important in helping categorize patients as low, moderate, or high risk for acute coronary syndrome, and performing a detailed history regarding chest pain complaints is critical. Low risk features include pleuritic, positional, reproducible, and sharp or stabbing pain. In addition, non-exertional pain and pain localized to a small inframammary area have a low likelihood of being cardiac in etiology. High risk features include chest pressure (positive likelihood ratio [LR+] 1.3), pain similar to prior cardiac pain (LR+ 1.8), and associated vomiting or diaphoresis (LR+ 1.9 and 2.0, respectively). The highest risk features include radiation to the right arm or shoulder (LR+ 4.7), left arm (LR+ 2.3), or both arms or shoulders (LR+ 4.1), and exertional chest pain (LR+ 2.4). Of the above choices, radiation to the right arm is the strongest predictor of a cardiac etiology of chest pain.
History of diabetes, hypertension, and tobacco use (A) are traditional cardiac risk factors that predict the lifetime risk of developing coronary artery disease. However, these risks factors are less helpful than historical features in predicting whether an acute presentation of chest pain is due to acute coronary syndrome. Pleuritic pain (B) is not a strong predictor of acute coronary syndrome. Pressure-like pain (C) is a high-risk feature but is less predictive or acute coronary syndrome than pain that radiates to the right arm.
[/toggle]
[/accordion]
References:
