High sensitivity cardiac troponins for ED chest pain evaluation (2022 ACC pathway)

How do we best use high-sensitivity cardiac troponin (hs-cTn) to risk stratify patients with symptoms concerning for an acute myocardial infarction (AMI)? The 2022 American College of Cardiology (ACC) pathway provides timely guidance [1]. We help you translate this to your clinical practice, by illustrating with a case. Time to know your hs-cTn better.

Take-to-work points

  • When interpreting the hs-cTn, you can use either of the following pathways to optimize both accuracy and patient throughput:
    • European Society of Cardiology (ESC) 2020 0/1 hour or 0/2 hour pathway
    • High-Sensitivity Troponin in the Evaluation of Patients With Acute Coronary Syndrome (High-STEACS)
  • These clinical decision pathways utilizing hs-cTn are complicated to calculate on your own.
    • Encourage your ED to set up an algorithm that you can follow based on your laboratory’s assay.
    • Otherwise, apply a simplified approach. When patients present with <6 hours of symptoms, they are low risk if the 0- and 3-hour troponin levels are less than the 99th percentile upper reference limit (URL).
  • Low-risk patients do not routinely require stress testing in the ED.
  • Intermediate-risk patients may be further stratified based on recent stress testing or coronary angiogram findings plus a modified HEART or Emergency Department Assessment of Chest Pain (EDACS) score.

Applying the 2022 ACC guideline

Before delving into the specifics of the hs-cTn pathways, start with the ECG. The ACC 2022 pathway has a section dedicated to ECGs in ischemia [1], and FOAMcast has a great visual summary.

The 2022 ACC pathway [1] endorses clinical decision pathways that:

  • Use hs-cTn AND
  • Enable rapid rule-out using very low hs-cTn values (far below the 99th percentile) on arrival, or a very small change (delta) between 2 hs-cTn values.

Examples of such pathways include [2]:

  • The ESC 0/1 hour pathway, where hs-cTn is obtained on arrival, and if needed, 1 hour later.
  • The ESC 0/2 hour pathway, where hs-cTn is obtained on arrival, and if needed, 2 hours later.
  • The High STEACS pathway, where hs-cTn is obtained on arrival, and if needed, 3 hours later.

These clinical decision pathways take advantage of the diagnostic power of the delta hs-cTn value, resulting in higher sensitivity for AMI (99%) [3], more patients being able to be ruled-out for AMI [4], and more patients being discharged home with a shorter ED length of stay [5]. This contrasts traditional risk-stratification approaches, which compare hs-cTn values solely to the 99th percentile upper reference limit.

  • Note: Using the pathways and using a single hs-cTn result are not mutually exclusive concepts. Clinical decision pathways DO allow us to rule out AMI with a single hs-cTn value in some instances. An example is if the patient has a very low value (e.g., below limit of detection) AND the chest pain onset is >3 hours ago AND the ECG is non-ischemic.

Let’s apply the ESC 2020 0/1 hour pathway [2], with some modifications based on the 2022 ACC guidelines [1]:

high sensitivity cardiac troponin hs-cTn risk stratification

Figure 1. Stratification of patients for AMI based on high sensitivity troponin testing and the ESC 0/1 hour pathway (second hs-cTn drawn 1 hour after the initial hs-cTn test)

Notice how numbers are replaced with values A, B, C, D and E. That’s because these values are assay specific. You (or someone in your department) needs to know which assay your ED has, and use the appropriate values for that assay. Examples of cutoffs:

Figure 2: Assay-based cutoffs for different high sensitivity cardiac troponin tests from the 2022 ACC guideline [1] (Limit of quantification, LoQ)

One concept that cuts across all assays is the limit of quantification (LoQ). That’s the lowest hs-cTn value that can be reliably reported as a number for that assay. In the risk stratification pathway (figure 1), value E is often the LoQ, or an optimized threshold slightly above the LoQ.

Case #1

A 52-year-old woman presents with vague heaviness over the left side of the chest that does not radiate elsewhere. She does not recall clearly how it started, and it has been persistent for 5 hours. Its intensity does not change with walking or changes in posture. There are no associated symptoms such as diaphoresis, breathlessness, vomiting, fever, cough, or leg swelling.

She has hypertension and hyperlipidemia treated with lifestyle modification. She does not smoke. There is no family history of heart disease. She has no other recent illnesses or travel history.

On examination, her vital signs are normal. Heart sounds are dual with no murmurs and breath sounds are equal bilaterally. Pulses are well felt in all four limbs. There is no lower limb swelling or tenderness.

A 12-lead electrocardiogram (ECG) and chest x-ray (CXR) are unremarkable. The hs-cTn level on arrival is below the limit of quantification (LoQ).

Because the patient’s chest pain started >3 hours ago and she has a non-ischemic ECG, the initial hs-cTn is below LoQ already stratifies her as a LOW-RISK patient for AMI by the pathway. She does not need a repeat hs-cTn test. Caveat: Patients with known coronary artery disease might still have considerable risk for AMI even with this constellation of findings, requiring clinical judgment beyond this pathway [6].

Also do not forget that you still need to address other important potential causes of chest pain:

  • Aortic dissection appears unlikely, given the lack of suggestive features on history or physical examination. The onset was gradual with no radiation to the back or abdomen, and no features of distal ischemia such as neurological or pulse deficits. The CXR did not show any abnormalities consistent with a dissection.
  • Pulmonary embolism (PE) appears unlikely. She would be low risk by gestalt or structured scoring systems (Wells or revised Geneva), and a negative D-dimer would essentially rule out pulmonary embolism here. Note that the PE rule-out criteria do not help in this case, because she is >50 years old.

Thankfully, most patients will be low risk after walking through the above. What’s the disposition and follow-up plan for them? In short, less is more. As long as your clinical judgment concurs with a low-risk stratification, you should send the patient home with chest pain advice, return precautions, and recommendations to follow-up with their primary care provider within 30 days for optimal management of cardiovascular risk factors. You do not have to routinely order stress testing from the ED! This is endorsed in the 2022 ACC pathway [1] and the 2021 AHA chest pain guidelines [7].

The high-risk category

High-risk category hs-cTn values in the ESC 2020 0/1 hour pathway or high STEACS pathway come in 2 types:

  • A high absolute value
  • A high delta between two hs-cTn samples, which is suggestive of the rise or fall seen in AMI

Those values are assay- and pathway-specific, so you’ll need to find out more about your local assay. These in the high-risk category are usually admitted to the hospital to assess for AMI as well as other causes of troponin elevation.

What if you have a patient with intermediate findings?

Case #2

A 66-year-old man with hypertension, hyperlipidemia, diabetes mellitus, and chronic renal failure presents with poorly localized central chest discomfort while trying to sleep. It started 2 hours ago. The discomfort has a burning character, though he has never been diagnosed with reflux before.

His vital signs and physical exam are unremarkable other than an arteriovenous fistula on his left arm for hemodialysis. His ECG shows left ventricular hypertrophy.

The first hs-cTn results in the intermediate range on your assay-specific cutoff for the ESC 2020 pathway or high-STEACS pathway.

The first step is to repeat hs-cTn testing in 3-6 hours. Those with a significant change in hs-cTn (e.g., ≥ value D in the ESC 2020 pathway) will be diagnosed with acute myocardial infarction or acute myocardial injury (e.g., as seen in heart failure, arrhythmias, or sepsis).

How about those with no significant change? The ACC now endorses that these intermediate-risk patients can be considered for discharge with rapid follow-up, if 1 of these 4 criteria are met:

  1. Invasive or CT coronary angiogram <2 years ago without coronary plaque
  2. Stress test <1 year ago without ischemia
  3. Modified HEART score (where troponin is excluded) ≤3 [MDCalc] or EDACS<16 [MDCalc]
  4. Chronic elevations in hs-cTn similar to previously measured levels

Patients who do not meet these criteria above should get some form of additional evaluation such as non-invasive testing, such as a CT coronary angiogram, myocardial perfusion imaging, or stress echocardiography. If not, consider cardiology consultation or admission, or at least a shared decision-making with the patient for an expedited outpatient workup with the understanding that this group has a 30-day rate of death or MI ranging from 5% to 22% [1, 8, 9].

You repeat a hs-cTn 3 hours later and it remains unchanged. The patient has no previous stress testing or coronary angiogram, and he is not low risk by HEART or EDACS scoring.

You thus consult the cardiologist, who recommends to admit the patient to the hospital for further observation and evaluation.

References

  1. Writing Committee, Kontos MC, de Lemos JA, et al. 2022 ACC Expert Consensus Decision Pathway on the Evaluation and Disposition of Acute Chest Pain in the Emergency Department: A Report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. 2022;80(20):1925-1960. doi:10.1016/j.jacc.2022.08.750
  2. Collet JP, Thiele H, Barbato E, et al. 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation [published correction appears in Eur Heart J. 2021 May 14;42(19):1908] [published correction appears in Eur Heart J. 2021 May 14;42(19):1925] [published correction appears in Eur Heart J. 2021 May 13;:]. Eur Heart J. 2021;42(14):1289-1367. doi:10.1093/eurheartj/ehaa575
  3. Burgos LM, Trivi M, Costabel JP. Performance of the European Society of Cardiology 0/1-hour algorithm in the diagnosis of myocardial infarction with high-sensitivity cardiac troponin: Systematic review and meta-analysis [published online ahead of print, 2020 Jun 29]. Eur Heart J Acute Cardiovasc Care. 2020;2048872620935399. doi:10.1177/2048872620935399
  4. Badertscher P, Boeddinghaus J, Twerenbold R, et al. Direct Comparison of the 0/1h and 0/3h Algorithms for Early Rule-Out of Acute Myocardial Infarction. Circulation. 2018;137(23):2536-2538. doi:10.1161/CIRCULATIONAHA.118.034260
  5. Chew DP, Lambrakis K, Blyth A, et al. A Randomized Trial of a 1-Hour Troponin T Protocol in Suspected Acute Coronary Syndromes: The Rapid Assessment of Possible Acute Coronary Syndrome in the Emergency Department With High-Sensitivity Troponin T Study (RAPID-TnT) [published correction appears in Circulation. 2021 Jun 22;143(25):e1118]. Circulation. 2019;140(19):1543-1556. doi:10.1161/CIRCULATIONAHA.119.042891
  6. Ashburn NP, Snavely AC, O’Neill JC, et al. Performance of the European Society of Cardiology 0/1-Hour Algorithm With High-Sensitivity Cardiac Troponin T Among Patients With Known Coronary Artery Disease. JAMA Cardiol. 2023;8(4):347-356. doi:10.1001/jamacardio.2023.0031
  7. Gulati M, Levy PD, Mukherjee D, et al. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines [published correction appears in Circulation. 2021 Nov 30;144(22):e455]. Circulation. 2021;144(22):e368-e454. doi:10.1161/CIR.0000000000001029
  8. Mueller C, Giannitsis E, Christ M, et al. Multicenter Evaluation of a 0-Hour/1-Hour Algorithm in the Diagnosis of Myocardial Infarction With High-Sensitivity Cardiac Troponin T. Ann Emerg Med. 2016;68(1):76-87.e4. doi:10.1016/j.annemergmed.2015.11.013
  9. Twerenbold R, Neumann JT, Sörensen NA, et al. Prospective Validation of the 0/1-h Algorithm for Early Diagnosis of Myocardial Infarction. J Am Coll Cardiol. 2018;72(6):620-632. doi:10.1016/j.jacc.2018.05.040

Featured image adapted from Adobe Firefly

SAEM Clinical Images Series: Wolf in Sheep’s Clothing

wolf

A 55-year-old female with a history of hyperlipidemia presents after a syncopal episode. She had mild nausea and diarrhea on the morning of presentation but otherwise had no prodromal symptoms before suddenly losing consciousness in a grocery store. Of note, she recalls a similar syncopal episode in the remote past, also preceded by gastrointestinal symptoms at that time. At present, she is symptom-free.

Vitals: BP 135/71; HR 52; Temp 98°F; RR 18; SpO2 100% on room air

General: Tired appearing

CV: 2+ peripheral pulses. Regular rate and rhythm, no murmurs, rubs, or gallops.

Pulmonary: No increased work of breathing. Lungs clear to auscultation bilaterally.

GI: Soft, non-distended, non-tender to palpation.

Non-contributory

Wolff-Parkinson-White Syndrome (WPW)

Short PR interval (< 0.12 seconds) and slowed upstroke of the QRS complex, referred to as a delta wave, which are both seen in our patient. These particular EKG findings define a “Wolff-Parkinson-White Pattern.”

WPW is a pre-excitation syndrome characterized by an accessory pathway caused by a congenital failure of cells to resorb near the AV valves. This accessory pathway conducts impulses faster than the AV node, causing a short PR interval. WPW Syndrome consists of characteristic EKG findings as well as symptomatic arrhythmias. Patients with WPW may classically present after a syncopal episode due to an arrhythmia involving the accessory pathway. Most commonly, WPW is associated with atrioventricular nodal reentrant tachycardia (AVNRT) and atrial fibrillation.

First-line treatment for WPW-mediated tachyarrhythmia consists of procainamide, which blocks conduction through the accessory pathway. An exception to this would be the hemodynamically unstable patient, who should be cardioverted. AV nodal blocking agents should be avoided in patients with tachyarrhythmias as they can cause increased conduction to the ventricles through the accessory pathway, leading to potential ventricular arrhythmias and hemodynamic instability. Ablation of the accessory pathway is indicated in those with symptomatic tachyarrhythmias and leads to successful remission in about 90 percent of cases.

Take-Home Points

  • The WPW pattern on EKG consists of a short PR interval and a delta wave.
  • Patients with WPW Syndrome classically present with symptomatic arrhythmias (including syncope) and EKG findings consistent with WPW pattern.
  • The most common arrhythmias seen in WPW include AVNRT and atrial fibrillation, which should be managed with procainamide. Avoid the use of AV nodal blocking agents.

  • Conover MB. Diagnosis and management of arrhythmias associated with Wolff-Parkinson-White syndrome. Crit Care Nurse. 1994 Jun;14(3):30-9; quiz 40-1. PMID: 8194348.
  • Dagres N, Clague JR, Kottkamp H, Hindricks G, Breithardt G, Borggrefe M. Radiofrequency catheter ablation of accessory pathways. Outcome and use of antiarrhythmic drugs during follow-up. European heart journal. 1999 Dec 1;20(24):1826-32.
  • Wolff L, Parkinson J, White PD. Bundle-branch block with short P-R interval in healthy young people prone to paroxysmal tachycardia. 1930. Ann Noninvasive Electrocardiol. 2006 Oct;11(4):340-53. doi: 10.1111/j.1542-474X.2006.00127.x. PMID: 17040283; PMCID: PMC6932258.

By |2023-11-12T13:55:35-08:00Nov 6, 2023|Cardiovascular, ECG, SAEM Clinical Images|

Trick of Trade: Alternative to a Pressure Bag for IV Fluids

pressure bag IV fluidsYou have a severely dehydrated patient with a peripheral IV line, requiring urgent fluid resuscitation. However, the crystalloid fluids are not flowing freely. Multiple attempts were made to place this line with the latest having a flash of blood return and a smoothly flowing saline flush. You can not seem to find your pressure infusion cuff to squeeze the IV bag and accelerate fluid administration.

Trick of the Trade: Manually provide positive pressure fluids using a 3-way stopcock

  1. Attach a 3-way stopcock between the angiocatheter and IV tubing.
  2. In the unused port, attach a 10 or 20 cc syringe.
  3. Fill the syringe with fluids from the IV bag (turn off flow to the angiocatheter using the stopcock)

Trick of the trade stopcock pressure infusion IV fluids syringe start

  1. Rotate the stopcock 180-degrees and push the syringe fluid into the angiocatheter.

Trick of the trade stopcock pressure infusion end

  1. Repeat this process several times.
  2. After manually pushing 100-200 cc of fluid through the line, turn the stopcock to shut off the syringe port. The fluids should flow more rapidly with gravity alone.

Word of Caution: Syringe Fluid Contaminant

Thanks to Twitter feedback from @cpatrick_89, be careful of introducing bacteria when attaching these pieces to the IV tubing, based on an in vitro study. Wearing gloves helped reduce bacterial contamination [1].

Note that conventional pressure bags may not be readily available in emergency departments and could blow the line you worked hard to secure. This “gentle pressure” technique allows the clinician to gauge how much positive pressure to administer to minimize the risk of fluid extravasation.

Interested in Other Tricks of the Trade?

Reference

  1. Kawakami Y, Tagami T. Pumping infusions with a syringe may cause contamination of the fluid in the syringe. Sci Rep. 2021;11(1):15421. Published 2021 Jul 29. doi:10.1038/s41598-021-94740-1

SAEM Clinical Images Series: Incidental Finding on Bedside Echo

echo

A 48-year-old female with a past medical history of opioid use disorder on suboxone presents with abdominal pain for one day. The patient developed sharp diffuse upper abdominal pain the evening prior to arrival that resolved. The pain recurred again today and was associated with bilious emesis. The patient notes persistent upper abdominal pain with paroxysmal exacerbation. She has a history of a hysterectomy, but no other abdominal surgeries. No history of gallstone pathology.

Vitals: HR 38; BP 120/63; RR 14; SpO2 100%

HEENT: No jugular venous distention, no scleral icterus.

CV: Normal S1, S2, regular rhythm.

Respiratory: Clear breath sounds bilaterally.

Abdominal: Mild tenderness to palpation in the epigastrium, without rebound or guarding.

Extremities: Warm and well perfused, no edema.

White blood cell (WBC) count: 11

Alk phos: 123

Total Bilirubin: 0.5

Lipase: 24

Troponin: 0

Lactate: 1

An echo was performed for bradycardia and a brief episode of hypoxia in the emergency department. A large, tethered mass is seen likely originating from the left atrium. This finding is most consistent with an atrial myxoma, though it can also represent a clot. The patient was ultimately diagnosed with gallstone ileus and an atrial myxoma.

Take-Home Points

  • Myxomas are the most common type of cardiac mass. They occur more commonly in females, arising between the fourth and sixth decade of life. They are most commonly located in the left atrium.
  • Patients can experience obstructive and thromboembolic symptoms. Distal embolic events can cause neurologic deficit, visceral ischemia, STEMI, and limb ischemia amongst other critical presentatations.
  • Bernatchez, J., Gaudreault, V., Vincent, G., & Rheaume, P. (2018). Left atrial myxoma presenting as an embolic shower: a case report and review of literature. Annals of vascular surgery, 53, 266-e13.
  • Nguyen T, Vaidya Y. Atrial Myxoma. 2022 Jul 4. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan–. PMID: 32310500.

SAEM Clinical Images Series: Found Down

found down

A 67-year-old caucasian male experiencing homelessness was “found down” in a parking lot. EMS reported that he had a GCS of 6 with a systolic blood pressure in the 80’s, finger stick glucose of 100, and no response to intranasal naloxone. He was intubated in the field and arrived to the emergency department unresponsive with a BP of 95/60, HR 125, T 38°C, and O2 Sat 100%. Hemodynamic stabilization was achieved with central venous access, and laboratory and imaging studies for the evaluation of altered mental status ensued.

General: Disheveled male

HEENT: Normocephalic; PERRLA 3-2 mm; dried blood in nares

Skin: Warm; dry; no visible signs of trauma

Cardiovascular: Tachycardic with no murmurs, rubs, or gallops

Respiratory: Bilateral breath sounds on ventilator; diffuse rales

Gastrointestinal: Soft; non-distended; bowel sounds present

Musculoskeletal: No deformities

Neurologic: Unresponsive; GCS 3

COVID-19 rapid antigen: Detected

Complete Blood Count (CBC): WBC 17 k; Hemoglobin 15; Platelets 185

Comprehensive Metabolic Panel (CMP): Na 133; K 4.6; Cl 91; CO2 21; BUN 18; Cr 2.2; Ca 8.4; Alb 2.1; Tbili 0.4; Alk phos 112; AST 242; ALT 68

ABG on FiO2 100%: 6.99/>95/405/23/100%

Lactate: 16.4

Ammonia: 90

CK total: 716

Trop I HS: 809

PT: 14

INR: 1.05

PTT: 45

Urinalysis: Unremarkable

EtOH, Acetaminophen, Salicylate: Negative

UDS: Negative

Chest Radiograph: Diffuse ground-glass opacities

Air embolism to the right ventricle and pulmonary artery. As little as 20 mL or less of air rapidly infused may cause obstruction, ischemia, and hemodynamic collapse.

Risk factors include central venous catheterization, lung trauma, ventilator usage, hemodialysis, surgery (esp. coronary, neurosurgery), childbirth, and scuba diving barotrauma.

Take-Home Points

  • In the appropriate clinical scenario, especially those involving respiratory, cardiac, and neurologic findings where invasive procedures were utilized, the diagnosis of venous air embolism should be entertained.
  • Immediate management of an air embolism involves administration of 100% oxygen by nonrebreather mask (NRM) or ventilator and placement of the patient in the left lateral decubitus (Durant maneuver) and Trendelenburg positions. Hyperbaric oxygen therapy has also been used if there is no clinical improvement.
  • The purpose of the Durant maneuver and Trendelenburg position is to trap air along the lateral right ventricular wall, preventing right ventricular outflow obstruction and embolization into the pulmonary circulation.

  • Gordy S, Rowell S. Vascular air embolism. International Journal of Critical Illness and Injury Science. 2013;3(1):73. doi:10.4103/2229-5151.109428 Malik N, Claus PL, Illman JE, Kligerman SJ, Moynagh MR, Levin DL, Woodrum DA, Arani A, Arunachalam SP, Araoz PA. Air embolism: diagnosis and management. Future Cardiol. 2017 Jul;13(4):365-378. doi: 10.2217/fca-2017-0015. Epub 2017 Jun 23. PMID: 28644058.

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