Jason Brown

Stress testing: a beginner’s guide

Stress testing: a beginner’s guide Author: Jason Brown, Capt, USAF, MD (EM Resident Physician, University of Maryland) // Editor: Alex Koyfman, MD Stress tests are aptly named in that the goal is to cause a physiologic stress and to, through a variety of modalities, detect that stress’ impact on the myocardium. There are three major modes of stressing the patient: Exercise – either treadmill or supine bike Vasodilation – adenosine, dipyridamole, regadenoson Inotropy – dobutamine There are five different ways to detect stress on the myocardium: EKG *all modalities employ Echocardiography Radionuclide imaging – Thallium201, Technetium99M PET MRI Treadmill stress testing is the most common form of stress test that you will see as a direct extension of the ED.  It employs the Bruce protocol (starting at 1.7mph and 10% grade with increases in both every 3 minutes to a maximum heart rate of 85% (220-age)) while the patient wears an EKG.  Tests are positive if the patient has early chest pain, hyper-/hypotension, ST changes, or arrhythmia. Supine bike exercise testing allows for real-time echocardiography.  This provides an excellent option for patients with valvular disease and are functional but cannot use a treadmill. The vasodilatory stress tests use agents which increase coronary blood blow.  They work on the principle that diseased arteries are already maximally dilated and that there will be no further perfusion of their vascular territories when under stress.  A variety of detectors can be used to detect the difference between rest and stress phases. Vasodilation is contraindicated in patients with hypotension, high AV block, or bronchospasm No caffeine (12 hours), Cialis (72 hours), nitrates (48 hours), or calcium channel blockers (48 hours) prior to the test Dobutamine stress tests use the positive inotropic effects of dobutamine to increase the heart rate and elicit perfusion deficits in lieu of actual exercise.  There are a variety of protocols but the main goal is to achieve 85% of maximal heart rate (220-age) and to use a detector to examine the myocardium. Contraindicated in patients with arrhythmias, significant hypertension, or LV outflow obstruction. Must hold beta-blockers and calcium channel blockers 24 hours prior.  Detection of myocardial perfusion deficits The EKG is the most common modality for detection of ischemic changes. Consistent horizontal or down-sloping ST depressions in contiguous leads is considered positive. In patients that have known CAD or prior revascularization, an abnormal EKG, or a need for functional examination of the heart structures (valvular function, LVEF, etc) then imaging should be considered. There are four major imaging modalities: SPECT, ECHO, PET, MRI. Dobutamine is used in conjunction with echocardiography to evaluate function under stress.  New wall motion abnormalities are considered positive for flow-limiting disease.  Drawbacks include: technologist-dependent images and difficult interpretation in patients with baseline wall motion abnormalities and/or the obese. All three of the above vasodilators can be used with SPECT, PET, and MRI; deemed myocardial perfusion imaging.  All three of these imaging modalities attempt to detect perfusion deficits between rest and stress states.  These tests are generally used in patients which need investigations which are beyond the scope of the emergency department. Recommendations: Personally, when I am evaluating a patient in our clinical decision unit (CDU, observation unit) I use either: An EKG treadmill stress for low-intermediate risk ACS patients with normal initial and serial EKGs who can exercise. A supine bike ECHO for any patient that is low-intermediate risk who has an abnormal but nonischemic EKG who can exercise. A dobutamine stress ECHO for any patient with an abnormal EKG who cannot exercise. Any patient with CHF, known CAD, previous PCI/CABG, BBB, or congenital cardiac issue should be evaluated by a staff cardiologist. REFERENCES -Anderson KM, Murphy DL, Balaji M. Essentials of noninvasive cardiac stress testing. J Am Assoc Nurse Pract. 2014;26(2):59-69. -Gibbons RJ, Balady GJ, Bricker JT, et al. ACC/AHA 2002 guideline update for exercise testing: summary article. J Am Coll Cardiol 2002; 40:1531. -Hendel RC, Berman DS, Di Carli MF, et al. ACCF/ASNC/ACR/AHA/ASE/SCCT/SCMR/SNM 2009 Appropriate Use Criteria for Cardiac Radionuclide Imaging. J Am Coll Cardiol 2009; 53:2201. -ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography. J Am Soc Echocardiogr 2011; 24:229. -Douglas PS , Khandheria B, Stainback R. et al. ACCF / ASE / ACEP / AHA / ASNC / SCAI / SCCT / SCMR 2008 Appropriateness Criteria for Stress echocardiography. Circulation. 2008;117:1478‐1497 -Fraker TD Jr, Fihn SD, et al. Chronic Stable Angina Writing Committee: focused update of the ACC/AHA 2002 guidelines for the management of patients with chronic stable angina: J Am Coll Cardiol. 2007;50(23):2264. – http://www.ncbi.nlm.nih.gov/pubmed/24730402 – http://www.ncbi.nlm.nih.gov/pubmed/24211281 – http://www.ncbi.nlm.nih.gov/pubmed/23517258 – http://www.ncbi.nlm.nih.gov/pubmed/21908137

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Posterior Stroke, HiNTS exam

Author: Jason Brown, MD (EM Resident Physician, University of Maryland) // Editor: Alex Koyfman, MD Background Posterior strokes make up 1 in every 5 ischemic strokes in the US.  That equates to about 150,000 strokes per year involving the posterior circulation with an incidence of 18/100,000.  Bottom line: This is a common, emergent diagnosis that every EM physician should be familiar with. Anatomy Posterior circulation constitutes the vertebral arteries, basilar artery, and posterior cerebral arteries in addition to all minor perforators.  The vascular territory is quite large and perfuses the brainstem, a number of cranial nerve structures, the cerebellum, and the posterior portions of the cerebrum. Signs/Symptoms Classically, the “Five D’s” were used to describe the signs and symptoms of a posterior stroke:  dizziness, diplopia, dysarthria, dysphagia, dystaxia.  Additionally, you can have motor and/or sensory deficits, which mimic an anterior circulation stroke.  Finally, the clinical findings of “crossed syndromes,” makes the diagnosis very likely. The Diagnostic Dilemma Most of the stroke awareness initiative in this country is aimed at the identification of anterior strokes; most famously with the FAST mnemonic (Face drop, Arm droop, Speech disturbance).    Studies have shown that using these criteria alone will miss a majority of posterior strokes. Given such a wide range of presenting symptoms (some of which are very nonspecific), how does an EM physician make this diagnosis? Diagnostics First, you must have a high index of suspicion for any patient that presents with a new, focal neurologic deficit.  Your history and physical exam are invaluable. There are imaging modalities that can help you identify acute ischemic strokes; namely, CT angiography and MRI/MRA.  The problem here is that both of these studies take quite a bit of time and all CVAs are time-sensitive emergencies. HiNTS The HiNTS exam stands for: Head impulse testing, Nystagmus, and a Test of Skew.  This exam was designed by  Dr Dave Newman-Toker to differentiate central and peripheral causes of vertigo; a common presenting symptom for posterior CVA.  This quick battery of tests has been shown to have a 100% sensitivity and 96% specificity for posterior strokes when any one of the three tests are suggestive of a central cause of vertigo. [table id=5 /] http://content.lib.utah.edu/cdm/singleitem/collection/ehsl-dent/id/6 Things to Consider The HiNTS exam takes practice and expertise to properly administer AND interpret. You should have a high index of suspicion for posterior CVA in patients with vertigo or new neuro deficits. http://www.ncbi.nlm.nih.gov/pubmed/19762709 http://www.ncbi.nlm.nih.gov/pubmed/24127701 http://www.ncbi.nlm.nih.gov/pubmed/24920847 EMCrit 33 – Diagnosis of Posterior Stroke http://emcrit.org/misc/posterior-stroke-video/

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The Wheeze That Wasn't – An Observation on Enterovirus D-68

These children are often a mixed picture of viral bronchitis/bronchiolitis PLUS an asthma exacerbation. Treatment with albuterol, ipratropium, magnesium sulfate, steroids, fluids, etc are all reasonable and prudent in this population. If they begin to clinically improve within 30 minutes then you can feel good about soothing their reactive airways. However, they still have underlying viral issues which may require non-invasive positive pressure ventilation (either high-flow nasal cannula or BIPAP). If they do not improve within 30 minutes then you should begin to plan for IMC/ICU admission as these patients will require significant monitoring and respiratory support.

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Outpatient PE treatment

Editor’s note: This post was listed in the LITFL Review 153‘s “Best of #FOAMed” category.

Venous thromboembolism (VTE) (deep vein thrombosis or pulmonary embolism) has an incidence of roughly 1 in 1,000 with an incidence of PE with or without DVT of 2.3 per 10,000.

One major factor to consider is that VTE is much more common in the elderly and has a mortality highly associated with co-morbidities such as cancer and underlying cardiovascular disease.

In the distant past any diagnosis of DVT and/or PE would result in admission for heparin bridging to oral anticoagulation therapy. This was largely due to a fear that outpatient management would lead to an increase in fatal embolic or major bleeding events. However, there is a great amount of literature that has established the safety of outpatient management of “low-risk” DVT; outpatient treatment has become standard of care for these patients.

“Low-risk” patients were those with no prior VTE, no PE, no prior heparin use, and no confounding co-morbidities (cancer, infection, stroke, etc).

So what about PE?
If outpatient management is standard of care for a select group of DVT patients, then can we treat PE as an outpatient? […]

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