Tag Archives: Cardiology

Acute Valvular Emergencies: Pearls and Pitfalls

Authors: Jessica Zack, MD (EM Chief Resident at SAUSHEC, USAF) and Brit Long, MD (@long_brit, EM Attending Physician at SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

A 64-year-old male presents with sudden onset subjective fever/chills, dyspnea, weakness, and mild hemoptysis that began 2 hours prior to arrival. His VS include HR 104, BP 103/62, RR 24, O2 Sat 84% on RA, and T 99.6. On exam, you note bilateral rales R > L, a 4/6 diastolic murmur consistent with his known history of aortic regurgitation, and JVD without peripheral edema. His EKG is only significant for sinus tachycardia. You send labs that include a BNP and troponin and order a stat portable CXR which is pictured below. You subsequently order a CT scan of the chest and start him on NIPPV. You are initially considering PE, ACS, multi-lobar pneumonia, and acute heart failure syndrome … but is there something else you’re missing?

 screen-shot-2017-01-04-at-8-23-14-pm

The prevalence of valvular heart disease in the United States is estimated to be about 2.5% and increases in prevalence with age.1 Though patients with clinically evident valvular heart disease have a 3.2-fold increase risk for stroke and 2.5-fold increase risk for death,2 most valvular heart disease encountered in the emergency department is chronic and does not require emergency stabilization.3 This is vastly different than the rare patient presenting with an acute valvular emergency. Symptoms of an acute valvular emergency may include dyspnea, tachycardia, pulmonary edema, and rapid development of cardiogenic shock. Many of these symptoms are seen with various other diagnoses, and the biggest pitfall clinicians may experience is leaving acute valvular emergency off the differential for patients presenting with acute dyspnea.

Valvular emergencies can be broken down by type of valve: native or prosthetic.  Native valve emergencies are almost always the result of regurgitation, while acute prosthetic valve dysfunction may be the result of either regurgitation or stenosis.4  

Valvular Structure and Function:

The heart is composed of four valves: the mitral and tricuspid valves (atrioventricular valves) and the pulmonic and aortic valves (semilunar valves). These valves all open and close passively in response to changes in pressure and volume. The right side of the heart functions similarly to left except that these valves experience much lower pressures. Since most native valve emergencies involve the mitral and aortic valves, we will focus our discussion here.  Inscreen-shot-2017-01-04-at-8-23-01-pm a normally functioning heart, the aortic valve is open during ventricular systole. This allows blood to flow from the left ventricle into systemic circulation. Once the aortic root pressure supersedes that of the left ventricle, the three cusps of the aortic valve fold in, and valve closure occurs. This marks the beginning of ventricular diastole. During this phase of the cardiac cycle, the mitral valve opens allowing flow from the left atrium to the left ventricle. Filling of the left ventricle is completed after the atrial “kick” which provides 10-40 % of the left ventricular end-diastolic volume.5 This is followed by closure of the mitral valve, and the cycle begins again with ventricular contraction. The anterior and posterior leaflets of the mitral valve are supported by the papillary muscles and chordae tendinae during ventricular contraction and aid in the prevention of reverse flow in the left atrium.6

 

Acute Aortic Regurgitation

Pathophysiology:  Acute aortic insufficiency is typically the result of either acute aortic dissection or endocarditis.7 It has also been reported in the case of blunt chest trauma.8 In acute aortic regurgitation (AR), the left ventricle (LV) pathologically fills during ventricular diastole preventing forward flow from the left atrium (LA). This greatly reduces stroke volume and causes a compensatory tachycardia to maintain cardiac output. In the acute setting, this regurgitation is met by a relatively stiff LV and causes increased LV pressure. The increased pressure in the LV stifles flow from the left atrium (LA) and may cause pulmonary congestion.  In severe AR, increased LV pressure may cause early closure of the mitral valve prior to atrial systole and exacerbate pulmonary congestion as the atria contracts against a closed valve.9,10 When AR is severe enough, the decreased cardiac output leads to progressive hypotension, peripheral vasoconstriction, and cardiogenic shock.

History/Exam: These patients will typically present with sudden onset of dyspnea. Other significant historical features may include those associated with the underlying cause of their AR such as tearing chest pain in aortic dissection or fevers in the setting of endocarditis. Physical exam may reveal evidence of pulmonary edema and cardiogenic shock such as rales, JVD, hypotension, pallor, and diaphoresis.3,13  Don’t be fooled by the absence of the typical blowing diastolic murmur in this patient. Murmurs are created by the velocity of blood flow over the valve. This velocity is largely determined by pressure gradients. In the acute AR versus chronic AR, the LV is less compliant which lends to equalization of end diastolic pressure in the aorta and LV.10 With a decreased pressure gradient, your murmur will likely be softer and shorter. Throw in a noisy ED, tachycardia, tachypnea, and rales, and your murmur may be completely inaudible.

Treatment: Definitive treatment for severe acute AR is immediate surgical intervention. Mortality for acute type A aortic dissection is as high as 1-2% per hour for the first several hours.11 So, how do we keep them alive until the OR?

-Intubate if necessary

-Nitroprusside: Yes, their blood pressure is probably already low. Stay with me. Nitroprusside causes afterload reduction, decreased LV preload, and results in reduced regurgitant volume.12 If your patient is going downhill, consider simultaneously starting dobutamine.

-Dobutamine: This ionotropic agent helps to increase contractility and stroke volume. In combination with nitroprusside, you may be able to achieve increased forward flow and temporize the patient.4,13

-Don’t forget antibiotics in the setting of suspected endocarditis.

Treatment Pitfalls:
-Beta blockers: I know, they’re tempting. Especially if your patient is dissecting. Beta blockers are relatively contraindicated in the case of acute AR.4 Beta blockers will decrease reflex tachycardia, but that tachycardia is currently maintaining their cardiac output. Additionally, that decrease in heart rate will increase the time spent in diastole and cause more aortic regurgitation.4

-Aortic Balloon Counterpulsation: This is absolutely contraindicated.4,13 Remember, the balloon pump will inflate during diastole and definitively make the problem worse.

Acute Mitral Regurgitation

Pathophysiology: The most common cause of acute mitral regurgitation (MR) is rupture of chordae tendinae or papillary muscles from ischemia and is typically seen within the first week following a myocardial infarction.13 However, other causes include leaflet perforation from infective endocarditis, blunt chest trauma, and leaflet tethering in acute cardiomyopathies.3,4,14  In acute MR, blood flows back across the mitral valve during ventricular systole. This causes a precipitous decrease in cardiac output. Additionally, blood is flowing into an atrium with normal compliance. This often results in rapid onset of pulmonary edema. In some cases, unilateral pulmonary edema may be seen. Most commonly, this unilateral edema is isolated to the right side or right upper lobe due to the regurgitant jet, particularly from a posterior flail leaflet, being directed towards the right pulmonary vein.15,16

History/Exam: Like acute AR, acute MR frequently leads to overt cardiogenic shock. One key historical difference is that these patients typically present 2-7 days after acute MI.13  Patients with acute MR present with sudden onset of dyspnea from rapidly amassing pulmonary edema, as well as tachycardia.13  Since the atria has not had time to develop additional compliance like in chronic mitral regurgitation, expect left atrial pressures to be high. Again, without a significant pressure gradient across the valve, don’t be surprised if the typical high-pitched holosystolic murmur is absent. This is particularly true if your regurgitant jet is aimed posteriorly and you are auscultating anteriorly.

Treatment: In addition to treating any underlying ischemia if present, definitive treatment is operative management.

Similar temporizing measures as used in acute AR may be useful here, with a few differences.

-Positive pressure for respiratory failure.3

-Nitroprusside or nitrates for afterload reduction.3,4,13 Often other afterload reducing agents, such as nicardipine, are more readily available in the ED. There is little data available directly evaluating whether other afterload reducing agents have similar clinical effects as nitroprusside.

-Dobutamine for inotropic effects.3,13

-Aortic Balloon Counterpulsation: A balloon pump may provide some benefit here if surgical intervention is not readily available.4,13 This will increase forward flow, increase mean arterial pressure, decrease regurgitant volume, and decrease left ventricular filling pressures.3

-Antibiotics if endocarditis is suspected.

Critical Aortic Stenosis

Background: Aortic stenosis (AS) is most commonly caused by age-related calcific changes of a normal valve, calcification of a bicuspid aortic valve, or rheumatic heart disease.17 The difference between AS and the other native valve emergencies discussed in this article is that aortic stenosis develops over many years prior to symptoms onset.18 Even patients with severe aortic stenosis may never develop symptoms, and their estimated risk of sudden cardiac death is still 0.5%-1.0% per year.18 However, once symptom onset does occur, mortality rate rapidly increases. Seventy-five percent of patients will die within 3 years of symptom onset.19

screen-shot-2017-01-04-at-8-22-46-pmPathophysiology: Severe AS is characterized by a fixed outflow obstruction, and cardiac output is preload dependent.  Since severity increases over time, LV hypertrophy develops as a compensatory mechanism to maintain ejection fraction. Patients will often maintain a normal ejection fraction, but this is commonly associated with an overall decreased cardiac output due to decreased end diastolic volumes in the hypertrophied LV.18  LV hypertrophy itself reduces diastolic function and impairs coronary perfusion contributing to angina,19 one of the most common symptoms of AS.  Another common presenting symptom of AS is syncope during exercise. Though not completely understood, it is theorized that the high resistance across the aortic valve prevents the increase in cardiac output required to maintain normotension during exercise when peripheral vasodilation occurs.18 When the AS becomes severe enough, it can lead to severe LV dysfunction and acute heart failure.

History/Exam: The most common symptoms of severe AS are angina, syncope, and dyspnea.17,18 Since severe AS is a disease process that happens over time, you are more likely to appreciate the crescendo-decrescendo systolic ejection murmur. However, it may be absent in the critically ill patient.17 This murmur often radiates into the carotids. Additionally, you may see evidence of LV hypertrophy on EKG and cardiomegaly on CXR.  Occasionally, patients with severe AS will present with acute left ventricular dysfunction and signs and symptoms of acute heart failure such as dyspnea, pulmonary edema, JVD, and even cardiogenic shock.

Treatment: There are two types of AS patients generally encountered in the ED: patients who have the potential to be sick at any time and patients who are currently really sick.

Patients with symptomatic AS (potential to be sick):

-IV Fluids: overall, AS is preload dependent, and these patients may require IVF resuscitation to maintain cardiac output.17

-Inpatient admission for echocardiography and evaluation for surgical aortic valve replacement.17,20

Patients with severe AS and failing LV (currently really sick AS), consider the following:

-Nitroprusside:17,19 There is limited data supporting the use of nitroprusside infusion in patients with severe AS and MAP > 60mm Hg.21 In this subset of patients, there is some evidence to suggest nitroprusside will decrease afterload, improve systolic and diastolic function, and reduce myocardial ischemia.22 This newer data goes against traditional teaching that nitrates will cause decreased blood pressure and decreased coronary perfusion.21 This should be considered in patients who can be closely monitored in an ICU setting and in conjunction with cardiology and/or an intensivist.

-Ionotropic agents such as dobutamine.17

-Early consultation with cardiology: in some cases percutaneous balloon dilation may be performed as a temporizing measure in patients too ill to immediately receive aortic valve replacement.20

 Prosthetic Valve Emergencies

Acute Valve Thrombosis:  During the first three months following surgery, both mechanical and bioprosthetic valves are at the greatest risk for thrombosis and thromboembolic complications.23 However, this risk has a lifelong persistence for patients with a mechanical valve. Thrombosis of a mechanical valve can lead to acute regurgitation, acute stenosis, or both.4 In severe cases, patients will present with acute dyspnea, weakness, and cardiogenic shock. The preferred treatment for patients with acute valve thrombosis is surgery. However, there is some evidence to support the use of intravenous thrombolytics.24 This decision should be made in conjunction with a cardiologist and cardiothoracic surgeon.

Other complications: While acute thrombosis is typically seen with mechanical valves, other complications such as paravalvular regurgitation from suture failure or dehiscence from endocarditis is seen in both mechanical and bioprosthetic valves.4 Up to 6% of prosthetic valves will be complicated by endocarditis within 5 years.3 This finding is associated with an overall poor prognosis, as approximately one third of patients diagnosed with prosthetic valve endocarditis will die within one year of diagnosis.25 If there is suspicion for prosthetic valve endocarditis, blood cultures should be drawn, antibiotics started, and echocardiography and consult with cardiology should be obtained.

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Case Resolution:

The patient was admitted to the MICU and was later intubated for worsening respiratory distress.  He had an echo performed and was found to have new severe mitral regurgitation with a flail posterior leaflet, in addition to his known chronic aortic regurgitation. After his echo, he was immediately taken to the operating room and underwent uncomplicated valve replacement of both mitral and aortic valves. He recovered uneventfully and was subsequently discharged home.

 Key Takeaways:

-In patients presenting with sudden onset dyspnea, always keep a valvular emergency on the differential.

-Murmurs may not be audible in the acute setting.

-Definitive management is surgery more often than not, so get consultants on board early.

-If you have a sick patient with a native valve emergency consider nitroprusside +/- dobutamine.

-If present, don’t forget to treat the underlying cause of aortic regurgitation (aortic dissection, endocarditis), mitral regurgitation (ischemia, endocarditis), or prosthetic valve emergency (endocarditis, thrombosis).

 

References/Further Reading

  1. Nkomo, Vuyisile T., Julius M. Gardin, Thomas N. Skelton, John S. Gottdiener, Christopher G. Scott, and Maurice Enriquez-Sarano. “Burden of Valvular Heart Diseases: A Population-based Study.” The Lancet9540 (2006): 1005-011.
  2. Petty, G. W., B. K. Khandheria, J. P. Whisnant, J. D. Sicks, W. M. O’Fallon, and D. O. Wiebers. “Predictors of Cerebrovascular Events and Death among Patients with Valvular Heart Disease: A Population-Based Study.” Stroke11 (2000): 2628-635.
  3. Alley, William D., and Simon A. Mahler. “Chapter 54: Valvular Emergencies.” Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 8th ed. N.p.: McGraw Hill, 2015.
  4. Mcclung, John Arthur. “Native and Prosthetic Valve Emergencies.” Cardiology in Review1 (2016): 14-18.
  5. Alhogbani, Tariq, Oliver Strohm, and Matthias G. Friedrich. “Evaluation of Left Atrial Contraction Contribution to Left Ventricular Filling Using Cardiovascular Magnetic Resonance.” Journal of Magnetic Resonance Imaging4 (2012): 860-64.
  6. Perpetua, Elizabeth M., Dmitry B. Levin, and Mark Reisman. “Anatomy and Function of the Normal and Diseased Mitral Apparatus.” Interventional Cardiology Clinics1 (2016): 1-16.
  7. Roberts, W. C., J. M. Ko, T. R. Moore, and W. H. Jones. “Causes of Pure Aortic Regurgitation in Patients Having Isolated Aortic Valve Replacement at a Single US Tertiary Hospital (1993 to 2005).” Circulation5 (2006): 422-29.
  8. Baek, J. H., J. H. Lee, and D. H. Lee. “Acute Aortic Valve Insufficiency following Blunt Chest Trauma.” European Journal of Trauma and Emergency Surgery5 (2010): 499-501.
  9. Eusebio, Jose, Eric K. Louie, Lonnie C. Edwards, Henry S. Loeb, and Patrick J. Scanlon. “Alterations in Transmitral Flow Dynamics in Patients with Early Mitral Valve Closure and Aortic Regurgitation.” American Heart Journal5 (1994): 941-47.
  10. Rees, J. R., E. J. Epstein, J. M. Criley, and R. S. Ross. “HAEMODYNAMIC EFFECTS OF SEVERE AORTIC REGURGITATION.” Heart3 (1964): 412-21.
  11. Hamirani, Y. S., C. A. Dietl, W. Voyles, M. Peralta, D. Begay, and V. Raizada. “Acute Aortic Regurgitation.” Circulation9 (2012): 1121-126.
  12. Miller, Richard R., Louis A. Vismara, Anthony N. Demaria, Antone F. Salel, and Dean T. Mason. “Afterload Reduction Therapy with Nitroprusside in Severe Aortic Regurgitation: Improved Cardiac Performance and Reduced Regurgitant Volume.” The American Journal of Cardiology5 (1976): 564-67.
  13. Lefebvre, Cedric, James C. O’Neill, and David Cline. Atlas of Cardiovascular Emergencies. New York: McGraw-Hill Education, 2015.
  14. Smedira, Nicholas G., Magued Zikri, James D. Thomas, Michael S. Lauer, John J. Kelleman, and Patrick M. Mccarthy. “Blunt Traumatic Rupture of a Mitral Papillary Muscle Head.” The Annals of Thoracic Surgery5 (1996): 1526-528.
  15. Shin, Jeong Hun, Seok Hwan Kim, Jinkyu Park, Young-Hyo Lim, Hwan-Cheol Park, Sung Il Choi, Jinho Shin, Kyung-Soo Kim, Soon-Gil Kim, Mun K. Hong, and Jae Ung Lee. “Unilateral Pulmonary Edema: A Rare Initial Presentation of Cardiogenic Shock Due to Acute Myocardial Infarction.” Journal of Korean Medical Science2 (2012): 211.
  16. Young, Andrew L., Charles S. Langston, Robert L. Schiffman, and Michael J. Shortsleeve. “Mitral Valve Regurgitation Causing Right Upper Love Pulmonary Edema.” Texas Heart Institute Journal1 (2001): 53-56.
  17. Chen RS, Bivens MJ, Grossman SA. Diagnosis and Management of Valvular Heart Disease in Emergency Medicine. Emergency Medicine Clinics of North America. 2011;29(4):801-810. doi:10.1016/j.emc.2011.08.001.
  18. Carabello BA. Introduction to Aortic Stenosis. Circulation Research. 2013;113(2):179-185. doi:10.1161/circresaha.113.300156
  19. Carabello BA, Paulus WJ. Aortic stenosis. The Lancet. 2009;373(9667):956-966. doi:10.1016/s0140-6736(09)60211-7.
  20. Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;129(23):2440-2492. doi:10.1161/cir.0000000000000029.
  21. Khot UN, Novaro GM, Popović ZB, et al. Nitroprusside in Critically Ill Patients with Left Ventricular Dysfunction and Aortic Stenosis. New England Journal of Medicine. 2003;348(18):1756-1763. doi:10.1056/nejmoa022021.
  22. Popovic ZB. Effects of sodium nitroprusside in aortic stenosis associated with severe heart failure: pressure-volume loop analysis using a numerical model. AJP: Heart and Circulatory Physiology. 2004;288(1):H416-H423. doi:10.1152/ajpheart.00615.2004.
  23. Carnicelli, Anthony. “Anticoagulation for Valvular Heart Disease.” American College of Cardiology. N.p., 18 May 2015. Web. 05 Dec. 2016.
  24. Özkan, Mehmet, Cihangir Kaymaz, Cevat Kirma, Kenan Sönmez, Nihal Özdemir, Mehmet Balkanay, Cevat Yakut, and Ubeydullah Deligönül. “Intravenous Thrombolytic Treatment of Mechanical Prosthetic Valve Thrombosis: A Study Using Serial Transesophageal Echocardiography.” Journal of the American College of Cardiology7 (2000): 1881-889.
  25. Lalani, Tahaniyat. “In-Hospital and 1-Year Mortality in Patients Undergoing Early Surgery for Prosthetic Valve Endocarditis.” JAMA Internal Medicine16 (2013): 1495-503.

The Great and Powerful HEART Score: Does it have a weakness?

Authors: Brit Long, MD (@long_brit, EM Attending Physician at SAUSHEC), Josh Oliver, MD (EM Resident at SAUSHEC, USA), and Matthew Streitz, MD (EM Chief Resident at SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

A 52-year-old male presents with 6 hours of chest pain, radiating to the left shoulder and associated with shortness of breath. He has a history of hypertension.  His vital signs and ECG are normal. His initial troponin is normal. You consider entering him into your center’s chest pain pathway, with repeat troponin in two hours.

Chest pain is common in the ED; for the majority of physicians not a single shift will go by without managing at least one patient with chest pain. Approximately 10% of visits to an ED are due to chest pain.1,2 Fear of myocardial infarction often predominates for both patients and physicians.1,2 However, acute coronary syndrome (ACS) accounts for a minority of these patients. In fact, less than 1% of acute myocardial infarctions (MI) are missed by emergency physicians.3,4 Historically, physicians admitted patients with obvious disease (such as STEMI or non STEMI), while other patients underwent some form of further stress testing, either as an inpatient, outpatient dedicated clinic, or in an observation unit. We now know this further risk stratification in patients with negative biomarkers and unchanged ECG offers little, if any benefit.5,6  Testing can lead to over-diagnosis and over-treatment.

The majority of physicians feel a rate of < 1% or 1-2% is appropriate for missed major cardiovascular adverse event (MACE).4,7 Investigators have sought a tool to consistently and efficiently risk stratify patients to less than 1% risk of MACE.8-14  Patients in this low risk category could potentially be discharged directly from the ED. Prior risk scores or decision aids include the TIMI risk score and GRACE, for example.8-12 These scores were not derived for use in the undifferentiated chest pain patient in the ED, but rather for high risk patients to evaluate for the need for invasive therapy.8-12  They are also complex and difficult to use.

The HEART score and pathway have revolutionized care of chest pain patients in the ED.13-17 The introduction of the HEART score demonstrated ability to stratify a significant percentage of patients as low risk and appropriate for discharge, and the HEART pathway with the addition of repeat troponin further decreases the risk of missed ACS to less than 1%.13-17

Many centers use this pathway. However, are there potential weaknesses when using this score or pathway? This post will evaluate these potential weaknesses. But to look for weaknesses, first let’s evaluate the HEART score and pathway. The initial HEART score is shown below.13,14

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As you can see, the HEART score consists of age, risk factors, history, ECG, and troponin. Low risk patients, defined by points 0-3, demonstrate low rate of major cardiovascular adverse event (MACE). The original study evaluating the HEART score spanned three months in the Netherlands, finding one third of patients to be low risk.13  The MACE rate in the low risk group was 2.5%.  Since this initial study, the score has been repeatedly validated using multiple methods, with MACE rate less than 2%.14-16

The HEART pathway can further decrease the miss rate, evaluated by Mahler et al.17 This pathway uses a HEART score of 0-3 and negative troponins. Use of this pathway has repeatedly demonstrated ability to risk stratify a large percentage of patients as low risk appropriate for discharge (some studies 40%), with low rate of MACE (< 1%).17

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The HEART pathway has demonstrated its utility, but where can it go wrong?

#1: Risk Factors –

Classically, cardiac risk factors (diabetes, hypertension, smoking, hyperlipidemia, family history) have been used to predict the presence or absence of ACS in chest pain. These risk factors were derived in longitudinal studies and likely play little role in the assessment of the patient in front of you.18,19 Jayes et al. finds that no risk factor increases likelihood of ACS in women, while in men, only diabetes and family history increase likelihood.18 A study by Han et al. finds patients over age 65 years overwhelms any other risk factors for predicting ACS, while in patients less than 40, the number of risk factors contributes to risk of ACS.19

The patient may deny medical problems if they never visit a physician or primary care manager. This would potentially give them 0 points, categorized as low risk, no matter the other factors. The patient may not say they have hypertension, hyperlipidemia, or diabetes, but usually when you see an obese patient with BP of 180/90 and blood glucose level of 188, you know better.

Tip: If the patient is hypertensive or has abnormal serum glucose, assume they have these risk factors and score them appropriately. Remember, obesity is a risk factor in the HEART score, and known cardiac disease, cerebrovascular disease, or prior stroke is 2 points on the risk score.13-17

#2: ECG

Significant ST depressions, nonspecific repolarization abnormalities, and normal define the specific categories on the score. Just like above, dynamic ECG changes with no other points on the HEART score could provide a score of 2, which theoretically would place the patient in the low risk category. Approximately 8-11% of patients will demonstrate normal initial ECGs, and in patients with STEMI, up to one third will demonstrate findings on ECG by 30 minutes.20,21 Another potential weakness is misinterpretation of the ECG.

Tip: The ECG must be viewed systematically and thoroughly. Obtain an old ECG if at all possible to look for changes. Do not dismiss T wave changes (such as hyperacute T waves or inversions). These T wave changes must be taken seriously, and repeat ECGs are a necessity, as changes may not be present on the initial ECG.

#3: Troponin

An elevated troponin (2 points) with no other points would categorize the patient as low risk on the HEART score. However, troponin elevation should be considered high risk and criteria for admission. The HEART pathway with troponin elevation takes this into account, with positive troponin resulting in admission for the patient.

Tip: Elevated troponin equals admission. The HEART pathway takes this into account.

#4: Age

Patients greater than 65 years receive two points. However, if they receive 0 points in other categories, this results in a score of 2, which is low risk based on scoring. Progressing age has consistently proven to be a risk factor for ACS, and these patients may not present with chest pain.22 Be wary of the patient with dyspnea, nausea/vomiting, and fatigue who is older.22-27 Also be concerned about the younger patient (such as a 35-year-old) with no risk factors and a story strongly suggestive of ACS.

Tip: Older patients warrant caution. Many do not present typically with chest pain, diaphoresis, and vomiting. Dyspnea is more common. The key for older patients is atypical equals typical.22,27

#5: History

The original HEART score study by Six et al. utilized two investigators to classify patient history.13 Literature demonstrates the most predictive factors of ACS include diaphoresis with chest pain, nausea and vomiting, pain radiation to both arms or right shoulder, and exertional pain.23-26 Chest wall tenderness, pleuritic chest pain, sharp/stabbing chest pain, positional chest pain, and reproducible chest pain decrease the likelihood.23-26 Carefully take a history, and evaluate for these factors.

Tip: Though the prior factors (diaphoresis, vomiting, exertional pain, radiation to both arms/right shoulder) increase the likelihood of ACS, up to 1/3 of patients will present with dyspnea, fatigue, or nausea.27,28 Pay close attention to diabetics, older patients, women, and heart failure patients, as these groups can present atypically.22,27  Atypical presentations are associated with increased mortality.

#6: Gestalt

EM physicians go through extensive training, resulting in tremendous clinical experience and gestalt. How does gestalt compare to the HEART score? Mahler et al. in 2013 compared unstructured physician assessment, HEART score, and North American Chest Pain Rule, each with serial troponins (0 and 3 hrs).17 The HEART score classified 20% of patients as low risk (with 99% sensitivity) compared to gestalt categorizing 13.5% of patients as suitable for discharge (98% sensitivity).17 However, many institutions that utilize the HEART pathway incorporate clinical gestalt.

Tip: Your experience evaluating these patients is invaluable.7 If the HEART score says the patient is low risk but your gestalt says something different, discuss this with your admitting team and the patient. Many missed cases of ACS are associated with younger patients with no risk factors but a concerning story for cardiac etiology of their chest pain. The patient likely warrants admission in this setting.

#7: Follow up

Some institutions that utilize the HEART pathway and discharge patients with scores 0-3 attempt to have patients follow up with their primary care physician. Mahler et al.’s HEART pathway study encouraged follow up, but did not mandate it.17 As many know, follow up isn’t always possible. Patients with borderline scores (such as a score of 3), may not be able to see a primary care physician for another visit. However, the AHA/ACC recommend further stratification within 72 hours of discharge, though many are moving from this.29

Tip: Advise your patient to follow up, and document the discussion. Ensure return precautions are provided, and more importantly, that the patient verbalizes and understands these precautions.

 #8: Points 3 or 4

The dividing line for low risk is 3, while a score above 3 is moderate or high.13-17 The line between 3 or 4 points can be gray, dependent on which areas receive points. A history given 1 point may be 2 points based on the assessment of another physician. A study evaluating MACE rate for each number of points on HEART would provide valuable information on the score and pathway.

#9: Research Design

This post will not delve into the design of the HEART score/pathway trials, but several items should be considered. First is pathway adherence in the studies, as some nonadherence was observed. Another component is potential physician disagreement on scoring. Some studies do not list HEART interobserver agreement, while others state that physicians were notified if any disagreement occurred.

 

How can we improve on the HEART score?

The risk of ACS in patients admitted with chest pain, normal ECG, and negative troponin is close to 0.2%.3 The HEART pathway provides support for discharging patients with scores 0-3. Some have sought means of improving the score. One study modified the score by weighing male gender separately, as well as obtaining serial troponins and ECGs over 2 hours.30 This is known as the HEARTS(3) score. The S(3) correlates to sex, serial 2-hour ECG, and serial 2 hour delta troponin. Investigators also find that history highly suspicious of ACS (+LR 13) is much stronger than 3 or more CAD risk factors or age over 65 (+LR 1.4).30   Serial troponins and serial ECGs may improve miss rates, but most providers obtain serial ECG and troponins in patients with chest pain.

Further areas of study include disposition and medical decision making in patients with scores 4-6, or intermediate risk patients. These patients have approximately 12-16% risk of MACE.13-17 Does stress testing add to this population? The benefits of stress testing are controversial, and further risk stratification with these tests is difficult.

What about the use of coronary CTA in moderate risk patients? If this test demonstrates no disease (or less than 50%), the risk of ACS is very low.31-37 However, the majority of the literature has evaluated the use of CCTA in patients already at low risk for ACS.33-37  Perhaps a pathway using CCTA for patients with scores 4-6 may allow discharge and further risk stratification, but this requires more study.

 

Summary and Takeaways:

– The risk of ACS in patients with negative biomarkers and normal ECGs approaches 0.2%.

– Prior risk scores, such as TIMI and GRACE, provide little, if any benefit, in risk stratification for ED chest pain patients.

– The HEART score and pathway can risk stratify patients into three separate categories: low (0-3), moderate (4-6), and high score (> 7).

Low risk patients on the HEART pathway demonstrate likelihood of ACS that approaches < 1%, and it is easy to use in the ED.

Risk factors, history, ECG, troponin, follow up, gestalt, patients with points 3 or 4, and research design are areas of potential weakness.

– Further improvement of the HEART pathway at this time is difficult, but in patients at moderate risk, CCTA may hold promise for evaluation of risk. This requires further study.


References/Further Reading

  1. Bhuiya FA, Pitts SR, McCaig LF. Emergency department visits for chest pain and abdominal pain: United States, 1999–2008. NCHS Data Brief. 2010;(43):1–8.
  2. Pope JH, Aufderheide TP, Ruthazer R, et al. Missed diagnoses of acute cardiac ischemia in the emergency department. N Engl J Med. 2000;342(16):1163–1170.
  3. Weinstock MB, Weingart S, Orth F, et al. Risk for clinically relevant adverse cardiac events in patients with chest pain at hospital admission. JAMA Intern Med 2015;175: 1207-1212.
  4. Than M, Herbert M, Flaws D, et al. What is an acceptable risk of major adverse cardiac event in chest pain patients soon after discharge from the Emergency Department? A clinical survey. Int J Cardiol 2013;166:752-754.
  5. Kosowsky JM. Approach to the ED patient with ‘‘low-risk’’ chest pain. Emerg Med Clin North Am 2011;29:721–7.
  6. Lai C, Noeller TP, Schmidt K, King P, Emerman CL. Short-term risk after initial observation for chest pain. J Emerg Med 2003;25: 357–62.
  7. Kline J.A., Johnson C.L., Pollack C.V., et al: Pretest probability assessment derived from attribute matching. BMC Med Inform Decis Mak 2005; 5: pp. 26.
  8. Antman EM, Cohen M, Bernink PM, et al. The TIMI risk score for unstable angina/non-ST elevation MI: a method for prognostication and therapeutic decision making. JAMA. 2000;284(7):835–842.
  9. Cohen M, Demers C, Gurfinkel EP, et al. A comparison of low- molecular-weight heparin with unfractionated heparin for unstable coronary artery disease. N Engl J Med. 1997;337:447–452.
  10. Eagle KA, Lim MJ, Dabbous OH, et al. A validated prediction model for all forms of acute coronary syndrome: estimating the risk of 6-month postdischarge death in an international registry. JAMA. 2004;291(22):2727–2733.
  11. Lyon R, Morris AC, Caesar D, et al. Chest pain presenting to the Emergency Department – to stratify risk with GRACE or TIMI? Resuscitation. 2007;74(1):90–93.
  12. GRACE Investigators. Rationale and design of the GRACE (Global Registry of Acute Coronary Events) project: a multinational registry of patients hospitalized with acute coronary syndromes. Am Heart J. 2001;141:190–199.
  13. Six AJ, Backus BE, Kelder JC. Chest pain in the emergency room: value of the heart score. Neth Heart J 2008;16:191-6.
  14. Backus BE, Six AJ, Kelder JC, et al. Chest pain in the emergency room. A multicenter validation of the HEART score. Crit Pathw Cardiol 2010;9:164–9.
  15. Backus BE, Six AJ, Kelder JC, Bosschaert MA, Mast EG, Mosterd A, et al. A prospective validation of the HEART score for chest pain patients at the emergency department. Int J Cardiol 2013 Oct 3;168(3):2153-8.
  16. Mahler SA, Hiestand BC, Goff DC Jr, Hoekstra JW, Miller CD. Can the HEART score safely reduce stress testing and cardiac imaging in patients at low risk for major adverse cardiac events? Crit Pathw Cardiol 2011;10:128–133.
  17. Mahler SA, Riley RF, Hiestand BC, Russell GB, Hoekstra JW, Lefebvre CW. The HEART Pathway randomized trial: identifying emergency department patients with acute chest pain for early discharge. Circ Cardiovasc Qual Outcomes 2015 Mar;8(2):195-203.
  18. Jayes RL Jr, Beshansky JR, D’Agostino RB, Selker HP. Do patients’ coronary risk factor reports predict acute cardiac ischemia in the emergency department? A multicenter study. J Clin Epidemiol. 1992 Jun;45(6):621-6.
  19. Hans JH, et al. The role of cardiac risk factor burden in diagnosing acute coronary syndromes in the emergency department setting. Ann Emerg Med 2007;49(2):145.
  20. Welch RD, Zalenski RJ, et al. Prognostic Value of a Normal or Nonspecific Initial Electrocardiogram in Acute Myocardial Infarction. JAMA 2001;286(16):1977-1984.
  21. Riley RF, et al. Diagnostic time course, treatment, and in- hospital outcomes for patients with ST-segment elevation myocardial infarction presenting with nondiagnostic initial electrocardiogram: a report from the American Heart Association Mission: Lifeline program. Am Heart J 2013 Jan;165(1):50-6.
  22. Alexander KP, et al. Acute coronary care in the elderly, part I: Non-ST-segment elevation acute coronary syndromes. Circulation 2007;115:2549-2569.
  23. Body R, Carley S, Wibberley C, McDowell G, Ferguson J, Mackway-Jones K. The value of symptoms and signs in the emergent diagnosis of acute coronary syndromes. Resuscitation. 2010 Mar;81(3):281-6.
  24. Edwards M, Chang AM, Matsuura AC, Green M, Robey JM, Hollander JE. Relationship between pain severity and outcomes in patients presenting with potential acute coronary syndromes. Ann Emerg Med. 2011 Dec;58(6):501-7.
  25. Goodacre S, Locker T, Morris F, Campbell S. How useful are clinical features in the diagnosis of acute, undifferentiated chest pain? Acad Emerg Med. 2002 Mar;9(3):203-8.
  26. Panju AA, Hemmelgarn BR, Guyatt GH, Simel DL. The rational clinical examination. Is this patient having a myocardial infarction? JAMA. 1998 Oct 14;280(14):1256-63.
  27. Brieger D, et al. Acute coronary syndromes without chest pain, an underdiagnosed and undertreated high-risk group. Insights from the Global Registry of Acute Coronary Events. Chest 2004;126(2):461-9.
  28. Dorsh MF, et al. Poor prognosis of patients presenting with symptomatic myocardial infarction but without chest pain. Heart 2001;86(5):494-8.
  29. Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014;64(24):e139-e228.
  30. Fesmire FM, Martin EJ, Cao Y, Heath GW. Improving risk stratification in patients with chest pain: the Erlanger HEARTS3 score. Am J Emerg Med. 2012 Nov;30(9):1829-37.
  31. Montalescot G, Sechtem U, Achenbach S, et al. 2013 ESC guidelines on the management of stable coronary artery disease: the Task Force on the Management of Stable Coronary Artery Disease of the European Society of Cardiology. Eur Heart J 2013;34:2949–3003.
  32. Fihn SD, Gardin JM, Abrams J, et al., American College of Cardiology Foundation/American Heart Association Task Force. 2012 ACCF/AHA/ACP/AATS/PCnA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart dis- ease: a report of the American College of Cardiology Foundation/ American Heart Association task force on practice guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation 2012;126:e354–471.
  33. Achenbach S. Can coronary computed tomography angiography replace invasive angiography? Yes: it is all about finding the right test for the right person at the right time. Circulation 2015;131: 410–6. discussion 417.
  34. Stefanini GG, Windecker S. Can coronary computed tomography angiography replace invasive angiography? Coronary computed tomography angiography cannot replace invasive angiography. Circulation 2015;131:418–25. discussion 426.
  35. deFilippi CR, Rosanio S, Tocchi M, et al. Randomized comparison of a strategy of predischarge coronary angiography versus exercise testing in low-risk patients in a chest pain unit: in-hospital and long- term outcomes. J Am Coll Cardiol 2001;37:2042–9.
  36. Litt HI, Gatsonis C, Snyder B, et al. CT angiography for safe discharge of patients with possible acute coronary syndromes. N Engl J Med 2012;366:1393–403.
  37. Redberg RF. Coronary CT angiography for acute chest pain. N Engl J Med 2012;367:375–6.

Tachycardic Arrhythmias in Pregnancy: Management

Author: Jennifer Robertson, MD, MSEd (Assistant Professor, Emory University, Atlanta GA) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

Case 1: A 37 yo G1P0 female at approximately 17 weeks gestational age presents to the emergency department (ED) with a chief complaint of a racing heart.  She denies any past medical history. Her heart rate is 180 beats per minute (bpm) but otherwise her vital signs are within normal limits. She denies chest pain. Her electrocardiogram (EKG) is shown below:

ekg1

http://emedicine.medscape.com/article/156670-overview

Case 2:  A 21 year old G1P0 female at approximately 16 weeks gestational age presents with a chief complaint of syncope. She arrives to the ED with a complaint of lightheadedness but is alert and oriented and able to converse. She does complain of some mild chest pain. Her heart rate is 160 bpm and her blood pressure is 85/60 mmHg. Her other vital signs are within normal limits.

ekg2

http://lifeinthefastlane.com/ecg-library/rvo/

Case 3: A 40-year-old G4P3 female at approximately 12 weeks gestational age presents after feeling palpitations for the last several days. She denies chest pain, syncope or shortness of breath. She denies any past medical history and denies taking any medications. Her initial heart rate is 165 bpm (irregular) and her blood pressure is 130/80 mmHg. Her EKG is shown as follows:

ekg3

http://misc.medscape.com/pi/iphone/medscapeapp/html/A156670-business.html

Introduction

Compared to the non-pregnant population, cardiac arrhythmias are rare in pregnancy, with an incidence of about 1.2 per 1000 pregnant women (1). However, they can negatively affect the health of both the mother and child, especially if they lead to hypoperfusion. Thus, emergently addressing them is important. Additionally, it is important to understand that the management of arrhythmias in pregnancy may vary considerably from the non-pregnant patient due to the potential effects of anti-arrhythmic medications and electrical therapy with sedation (2). Thus, this is a brief review of the evaluation and management of the pregnant patient who may present to the emergency department with a tachy-arrhythmia. Pathologic bradycardia is very rare in pregnancy and will not be covered in this current article (3).

General Physiology: Brief Review

Arrhythmias in pregnancy can be due to a number of causes including congenital heart disease, channelopathies, and other structural heart diseases (3). Examples include Wolff Parkinson White Disease, pulmonary hypertension, Marfan syndrome with a dilated aortic root, arrhythmogenic right ventricular dysplasia, and even coronary artery disease (4,5).  They can also be due to reasons that are commonly seen in non-pregnant patients such as idiopathic, infection/sepsis, electrolyte abnormalities, medications, toxins, pulmonary emboli and hyperthyroidism (2,6,7). Similar the general population, these causes should also be considered when evaluating for the underlying cause of the arrhythmia (6, 7).

For some pregnant patients, an arrhythmia may be recurrent from a previously diagnosed cardiac disease or a first-time presentation. Due to the many physiologic changes and stresses on the cardiovascular system, pregnancy can provoke arrhythmias in some women with undiagnosed structural heart disease (s) (4). In addition, in women with known tachy-arrhythmias, pregnancy may cause an increased risk of recurrence or worsening of the dysrhythmia (3, 7). A thorough family and personal history of structural heart disease should be obtained in addition to a family history of sudden or unexplained death (3).

Palpitations are usually benign and life threatening arrhythmias are rare in pregnant patients (1, 3, 7, 8), but evaluation for more serious arrhythmia is always necessary from an emergency medicine standpoint. As previously mentioned, assessing for underlying reversible causes such as infection, hyperthyroidism and toxins is important. However, if no underlying cause can be found and/or if the patient is unstable, then medical and/or electrical management is warranted.

Unstable Rhythms

In any unstable patient, the American Heart Association (AHA) makes the following recommendations (all Level C recommendations-consensus opinion of experts, case studies or standard of care) (9):

(a) Place the patient in the full left lateral decubitus position to relieve aortocaval compression.

(b) Administer 100% oxygen by facemask to treat and prevent hypoxemia.

(c) Ideally, intravenous (IV) access should be established above the diaphragm to ensure that medications can be adequately distributed into the circulation (not obstructed by the gravid uterus)

(d) Evaluate for any underlying causes of the patient’s symptoms.

Please review the following article for any specifics about cardiac arrest in pregnancy:

Jeejeebhoy FM, Zelop CM, Lipman S, Carvalho B, Joglar J, Mhyre JM, Katz VL, Lapinsky SE, Einav S, Warnes CA, Page RL. Cardiac Arrest in Pregnancy A Scientific Statement From the American Heart Association. Circulation 2015; 132(18):1747-73.

However, just as in non-pregnant patients with an unstable tachycardia causing hemodynamic compromise, immediate direct current (DC) cardioversion is indicated (1, 2, 10, 11). Overall, DC cardioversion has been found to be safe in all trimesters of pregnancy, but it does carry a small risk of inducing a fetal arrhythmia (3). Therefore, it is strongly recommended that when possible, cardioversion should be conducted with concurrent fetal monitoring and emergency caesarean section (C-section) availability (1, 3, 6, 12).  Women in later stages of pregnancy should have their pelvis tilted to the left to relieve compression of the vena cava, however the process, including the dosing of electricity, is otherwise the same as in non-pregnant patients (3, 7, 13). Higher doses of energy (up to 360J) in refractory cases still remains safe for both the mother and fetus (13).

Medication options for sedation (for cardioversion):

This article is also not intended to be a review of safe sedation in pregnancy. However, some excellent articles on sedation in pregnancy include:

Neuman G, Koren G. MOTHERISK ROUNDS: Safety of Procedural Sedation in Pregnancy. J Obstet Gynaecol Can 2013; 35(2):168-73.

Shergill AK, Ben-Menachem T, Chandrasekhara V, et al. Guidelines for endoscopy in pregnant and lactating women. Gastrointest Endosc. 2012; 76(1):18-24.

Stable Tachyarrhythmias

The majority of arrhythmias during pregnancy are stable and can be managed with conservative therapies (7). Medication therapy should be considered in patients who are symptomatic and/or have tachyarrhythmias that may lead to negative hemodynamic or physiologic complications (7). Of course, any significant acute hemodynamic compromise should lead the provider to consider cardioversion, as mentioned in the above section (14)

In addition, as previously discussed, a thorough history and physical should be conducted to rule out any reversible causes of the arrhythmia such as a pulmonary embolism, hyperthyroidism, hemorrhage, or infections (). A history of prior episodes and/or a history of structural heart disease are also important to obtain. Once reversible causes are ruled out and a thorough history is obtained, a primary stable arrhythmia requiring drug therapy can be considered (3).

The risk of any medication on the mother and fetus should be reviewed prior to its administration. Most antiarrhythmic medications have not been systematically studied in pregnancy and thus, all should be viewed as potentially harmful in pregnancy (6, 15). Most of these drugs are labeled as a Food and Drug Administration (FDA) category C except for amiodarone and atenolol, which are labeled as category D (16). As a review, category C means that risk cannot be ruled out and any category C medication should be used only if the potential benefits outweigh any potential risks to the fetus. Category D means that there is evidence of risk. There may be a benefit of this drug but that patients should be informed of all risks of the drug prior to giving it (16).

It should be noted that as of June 2015, the FDA initiated a change to pregnancy category labeling and that the use of letters will be phased out. In place of letters, a narrative summary based on the risk of each medication will be provided (17). Any medications submitted to the FDA after June 30, 2015 will use the new format immediately and that any prior prescription medications approved after June 2001 will have new labeling within 3-5 years (17). So as of now, most of these antiarrhythmic medications are still under the old letter category labeling but may change in the future.

Teratogenic risk is also the highest in the first eight weeks after fertilization and thus, especially careful consideration should be given to women in early pregnancy who receive drug therapy (18). This is not to say there is no risk in the other stages of pregnancy, but the risk to the fetus is significantly reduced after the first eight weeks (18).

Finally, it should be remembered that many of the physiologic changes of pregnancy will affect drug metabolism (19). Some of these changes include increased plasma volume, reduction in plasma proteins, changes in renal clearance of drugs and altered gastrointestinal absorption (7, 19). Progesterone levels also increase, which can affect hepatic metabolism (7). Thus, administering the lowest effective dose of a medication is prudent in this patient population (7).

  1. Palpitations/Premature Ventricular Contractions

Palpitations are very common during pregnancy. Along with paroxysmal supraventricular tachycardia, premature atrial and ventricular beats are the most frequently seen arrhythmias in pregnancy (3, 14). Treatment is typically not necessary but in patients with unbearable symptoms, cardioselective beta blockers can be started, but preferably after the first trimester (6).

  1. Atrioventricular (AV) Nodal Re-entrant Tachycardia (AVNRT) and AV Re-entrant Tachycardia (AVRT):

The most common supraventricular tachycardia in pregnancy is AVNRT. AVNRT occurs when there are dual AV nodal pathways (slow and fast) that form a part of a re-entry circuit. The tachycardia is initiated when a premature beat is blocked in the fast pathway but conducts over the slow pathway (20). If there is enough time for the fast pathway to recover from its refractory period, then the slow pathway impulse (initiated by the premature beat) may conduct retrogradely over the fast pathway and cause the re-entry circuit (20).

AVNRT should not be confused with AVRT, which is the second most common supraventricular tachycardia in pregnancy (21). AVRT occurs in patients with WPW. In AVNRT, the accessory pathways are located within or near the AV node, while in AVRT, the accessory pathways are located in the AV valvular rings (22). The majority of patients will have the orthodromic form with anterograde conduction through the AV conduction system and retrograde conduction via the accessory pathway, which leads to a regular, narrow complex tachycardia. On occasion, antidromic conduction can occur and cause a wide complex tachycardia (Obel et al). If there is concomitant atrial fibrillation and it is conducted via the antidromic pathway, a wide complex, irregular tachycardia can occur (22).

If AVNRT or AVRT is rapid enough, hemodynamic instability can occur and thus, cardioversion may be necessary (1, 14, 21). However, the majority of patients will not have hemodynamic instability and thus, conservative or medication therapies can be initiated.

First line therapies for stable AVNRT in pregnancy (1, 3, 4, 6, 7, 14, 23):

  1. Vagal maneuvers such as carotid massage or the Valsalva maneuver.
  2. Adenosine: safe and should be the initial drug of choice. The initial standard doses are the same as in non-pregnant patients – 6mg and 12 mg. Adenosine has a short half live and does not cross the placenta. Minor effects in the mother may include transient bradycardia and dyspnea. Note adenosine can induce bronchospasm and should be a consideration if the patient has a history of asthma.
  3. Intravenous metoprolol or propranolol can be used if adenosine is ineffective. Beta blockers are considered safe in pregnancy but they have been associated with intrauterine growth retardation. Atenolol should never be given, however as it has been associated with fetal hypotonia, neonatal respiratory depression, low birth weight and hypoglycemia.
  4. Verapamil should be considered as a third line agent if the above medications are not effective. Doses up to 10mg can be given without affecting the fetal heart rate. Watch for hypotension in the mother, however.

First line therapies for stable AVRT in pregnancy (3, 6, 7, 14, 15, 18):

  1. Vagal maneuvers
  2. Adenosine: may be used but only in regular tachycardias. Patients who have orthodromic AVRT with concomitant atrial fibrillation should not receive adenosine or any other AV nodal blocking agent as this can potentially lead to accelerated conduction through the accessory pathway and lead to dangerous ventricular tachycardias.

AV nodal blocking agents including calcium channel blockers and digoxin should also be used with caution in patients with wide complex tachycardias of unknown pathogenesis.  Just as in non-pregnant patients, procainamide is the drug of choice in these circumstances.

  1. Procainamide: IV procainamide is safe in the short-term treatment of AVRT. It should be avoided in patients with underlying structural heart disease as it can be pro-arrhythmogenic. It should not be used long term as it can cause a lupus-like syndrome.
  1. Focal Atrial Tachycardia:

Focal atrial tachycardia (FAT) is usually associated with structural heart disease and is rarely seen in pregnancy (14). FAT can be difficult to treat as many are resistant to medications and even cardioversion (7, 15). The main objective is to control the maternal heart rate so that tachycardia-induced cardiomyopathy can be prevented. Adenosine should be attempted first as it is diagnostic and may, on occasion, terminate the arrhythmia (6). If adenosine does not work, the next recommended initial therapies are beta blockers, non-dihydropyridine calcium channel blockers or digoxin. Sotalol, flecainide or propafenone can be given if the beforementioned drugs do not work. Finally, amiodarone can be given but only in severe, refractory cases (7, 15).

  1. Atrial fibrillation/Atrial Flutter:

Unless there is underlying structural heart disease or hyperthyroidism, atrial flutter and atrial fibrillation are rarely seen during pregnancy (15, 21). However, if atrial flutter (AFL) or atrial fibrillation (AF) with a rapid ventricular response is present in pregnancy, serious hemodynamic effects can occur to both mother and fetus (15). Thus, urgent treatment is important in these patients.

Therapeutic options for stable patients with AFL or AF with rapid ventricular response:

  1. DC or pharmacologic cardioversion: similar to the non-pregnant population, stable pregnant patients who have had AFL or AF for > 48 hours duration will require 3 weeks of anticoagulation and/or a transesophageal echocardiogram to evaluate for a left atrial thrombus prior to the procedure (15). However, if the duration of the arrhythmia is less than 48 hours and the patient’s CHADS2-VASC score is < 2, post-cardioversion anticoagulation may not be necessary (7, 15). In this case, the patient should receive a dose of heparin or weight adjusted low molecular weight heparin (LMWH) prior to and during cardioversion (15). For patients who require anticoagulation after cardioversion, LMWH is the drug of choice (15). Warfarin can be used in the second and third trimesters but not in the first trimester or last month of pregnancy (6, 15). As of now, given the limited research, the new oral anticoagulants should not be used in pregnant patients (6, 15).

If pharmacologic cardioversion is considered, ibutilide or flecainide can be given but only in patients with structurally normal hearts (15, 21, 24). Ibutilide is particularly useful in treating AF in patients with pre-excitation syndromes. It can prolong the QT and thus, pre-treatment with magnesium is recommended (7). Again, amiodarone can be given but only as a last resort. There is less experience with propafenone so it should be avoided unless it must be used as a last resort as well (15).

  1. Rate control: For stable patients who are not candidates for cardioversion and/or have refractory AF or AFL, rate control is recommended (6, 7, 14, 15, 25). The AHA/ACC do not define what adequate rate control in pregnancy is, nor could any other literature be found regarding a goal maternal heart rate (26).

With the exception of atenolol, beta blockers are recommended as first line rate control medications in patients with rapid AF or AFL who do not have acute heart failure (6, 7, 14, 15, 25).Metoprolol 5mg IV over 5 minutes and repeated, if necessary, is an option for initial rate control (14). Verapamil, diltiazem and digoxin are second line agents (6, 14, 15, 25). Remember that these drugs should not be given if a pre-excitation syndrome is present.

  1. Ventricular Tachycardia:

Ventricular tachycardia (VT) is rare during pregnancy and inherited disorders should be considered when asking patients about their past medical and family histories (15). Some of the more common causes of VT in pregnancy may include idiopathic right ventricular (RV) outflow tract tachycardia, long QT syndrome, valvular heart disease and hypertrophic cardiomyopathy (3, 6, 15, 27). Rarely does ischemia cause a cardiomyopathy or arrhythmias in pregnant patients but coronary artery dissection or vasospasm has been known to occur in pregnant patients (6).  Post-partum cardiomyopathy should also be ruled out in women presenting with new onset VT during the last 6 weeks of pregnancy or in the early post-partum period (15).

The most important goal for pregnant patients with VT is timely conversion back to normal sinus rhythm because eventually, poor perfusion to both mother and fetus can occur (15).Just as in unstable supraventricular rhythms, acute treatment of any unstable VT should always be treated with DC cardioversion (15). Conversely, pharmacotherapy may be considered in pregnant patients with stable VT (6, 13, 15, 27). Importantly, any pregnant patient with a wide complex tachycardia should be evaluated by obstetric and cardiology specialists (18).

Idiopathic RV outflow tract tachycardia is one of the more common types of VT seen in pregnancy. It is almost always a stable tachycardia and most of the time, it is not sustained. The recommended treatment is beta blockade or verapamil. Idiopathic LV tachycardia is not as common but it responds well to verapamil (3, 15).

In pregnant patients with stable monomorphic VT, lidocaine, procainamide, or sotalol are recommend as first line agents (3, 15, 27).

Polymorphic VT is definitely most concerning as it has a higher likelihood of converting to ventricular fibrillation (3). Long QT syndrome should be a concern in patients with polymorphic VT and thus, all medications that may prolong the QT should be eliminated. In addition, treatment should include magnesium and correction of any electrolyte disturbances (3). Magnesium should be given at a dose of 1-2 grams IV over 1-2 minutes (13). It is controversial whether pregnant patients with long QT are at risk for VT during pregnancy, but it has been demonstrated that patients with long QT are definitely at an increased risk for arrhythmias post-partum (28, 29). Thus, any post-partum patient who presents in VT should have long QT syndrome as a possible etiology of her condition.

Conclusions

While there are a few differences, the management of tachycardic arrhythmias in pregnancy is quite similar to the non-pregnant patient. DC cardioversion should always be conducted in patients with hemodynamic instability. Pharmacologic cardioversion of supraventricular and ventricular arrhythmias is possible in the stable patient. No drugs are completely safe in pregnancy, but most are rated category C in pregnancy and if the benefit exceeds the risk, then the medication may be given.  Amiodarone and atenolol are two medications that should be avoided in the pregnant patient, especially in the first trimester. Rate control with beta blockers or calcium channel blockers is an option in patients with supraventricular tachycardias who are not immediate candidates for cardioversion. Stroke risk should still be accounted for and at risk patients should be anticoagulated with LMWH or vitamin K antagonists (only in the 2nd and 3rd trimesters and not in the last month of pregnancy). Finally, close cardiac monitoring of both the mother and fetus and availability of emergency C section should be available whenever medication or cardioversion is indicated. Finally, but importantly, obstetrics and cardiology consultation is prudent whenever a pregnant patient with an abnormal tachycardic arrhythmia presents to the ED.

Case Resolution

Case 1: The patient in this case has new onset AVNRT. Her electrolytes are normal, her thyroid function is normal, and her infection workup is negative.  Since her vital signs are otherwise stable and she denies chest pain, adenosine 6mg IV push is administered. Her rhythm returns back to normal sinus rhythm and she is discharged home with close cardiology and obstetrics follow up.

Case 2: This patient has unstable ventricular tachycardia. She is immediately cardioverted with direct current. She was ultimately found to have right ventricular (RV) outflow tract tachycardia. Obstetrics and cardiology were consulted and the patient was admitted for maternal and fetal cardiac monitoring. She was eventually discharged with a beta blocker for prophylaxis and cardiology follow up.

 Case 3: The last patient has atrial fibrillation with rapid ventricular response. Her workup for infection is also negative and her thyroid function tests and electrolytes are normal. Since her symptoms had been present for several days, rate control was chosen. Metoprolol was given and she achieved adequate rate control. She was admitted for a transesophageal echo prior to cardioversion and eventually she was cardioverted back to normal sinus rhythm.

References/Further Reading

  1. Tromp CH, Nanne AC, Pernet PJ, Tukkie R, Bolte AC. Electrical cardioversion during pregnancy: safe or not? Neth Heart J 2011;19(3):134-6.
  2. Ferrero S, Colombo BM, Ragni N. Maternal arrhythmias during pregnancy. Arch Gynecol Obstet 2004; 269(4):244-53.
  3. Adamson DL, Nelson-Piercy C. Managing palpitations and arrhythmias during pregnancy. Heart. 2007; 93(12):1630-6.
  4. Newstead-Angel J, Gibson PS. Cardiac drug use in pregnancy: safety, effectiveness and obstetric implications. ExpertRev Cardiovasc Ther 2009; 7(12):1569-80.
  5. Gaiser R. Physiologic changes of pregnancy. Chestnut’s obstetric anesthesia: Principles and practice. 2009;4:15-36.
  6. Enriquez AD, Economy KE, Tedrow UB. Contemporary management of arrhythmias during pregnancy. Circ Arrhythm Electrophysiol 2014;7(5):961-7.
  7. Burkart TA, Miles WM, Conti JB. Principles of Arrhythmia Management During Pregnancy. Cardiovascular Innovations and Applications. 2016;1(2):143-55.
  8. Joglar JA, Page RL. Management of arrhythmia syndromes during pregnancy. Curr. Opin. Cardiol. 2014; 29(1):36-44.
  9. Jeejeebhoy FM, Zelop CM, Lipman S, Carvalho B, Joglar J, Mhyre JM, Katz VL, Lapinsky SE, Einav S, Warnes CA, Page RL. Cardiac Arrest in Pregnancy A Scientific Statement From the American Heart Association. Circulation. 2015;132(18):1747-73.
  10. Petrescu V, Petrescu M, Bogdan S. Arrhythmias in Pregnancy-one case report and current recommendations from a cardiological perspective. GINECO RO 2010; 6(2):124-7.
  11. Crijns HJ. Electrical cardioversion in healthy pregnant women: safe yes, but needed? NethHeartJ 2011; 19(3):105-6.
  12. Barnes EJ, Eben F, Patterson D. Direct current cardioversion during pregnancy should be performed with facilities available for fetal monitoring and emergency caesarean section. BJOG 2002; 109(12):1406-7.
  13. Trappe HJ. Emergency therapy of maternal and fetal arrhythmias during pregnancy. J EmergTraumaShock 2010; 3(2):153.
  14. Knotts RJ, Garan H. Cardiac arrhythmias in pregnancy. In Seminars in perinatology 2014 (Vol. 38, No. 5, pp. 285-288). WB Saunders.
  15. Regitz-Zagrosek V, Lundqvist CB, Borghi C, Cifkova R, Ferreira R, Foidart JM, Gibbs JS, Gohlke-Baerwolf C, Gorenek B, Iung B, Kirby M. ESC Guidelines on the management of cardiovascular diseases during pregnancy. EurHeartJ 2011:ehr218.
  16. Food and Drug Administration; Accessed Nov 15, 2016: www.fda.gov.
  17. Food and Drug Administration. Content and format of labeling for human prescription drug and biological products; requirements for pregnancy and lactation labeling. Federal registrar 2014; Vol. 79 (233): 72064-72103.
  18. Page RL. Treatment of arrhythmias during pregnancy. AmHeartJ 1995;130(4):871-6.
  19. Cox JL, Gardner MJ. Treatment of cardiac arrhythmias during pregnancy. Prog Cardiovasc Dis. 1993; 6(2):137-78.
  20. Kwaku KF, Josephson ME. Typical AVNRT—an update on mechanisms and therapy. Card Electrophysiol Rev. 2002; 6(4):414-21.
  21. Merino JL, Perez-Silva A. Tachyarrhythmias and Pregnancy.
  22. Obel OA, Camm AJ. Accessory pathway reciprocating tachycardia. EurHeartJ 1998; 19:E13-24.
  23. Elkayam U, Goodwin TM. Adenosine therapy for supraventricular tachycardia during pregnancy. Am J Cardiol 1995; 75(7):521-3.
  24. Kockova R, Kocka V, Kiernan T, Fahy GJ. Ibutilide‐Induced Cardioversion of Atrial Fibrillation During Pregnancy. J Cardiovasc Electrophysiol. 2007;18(5):545-7.
  25. Cacciotti L, Passaseo I. Management of Atrial Fibrillation in Pregnancy. J AtrFibrillation 2010;2(2).
  26. Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH, DeMets D, Guyton RA, Hochman JS, Kovacs RJ, Ohman EM. Management of patients with atrial fibrillation (compilation of 2006 ACCF/AHA/ESC and 2011 ACCF/AHA/HRS recommendations): a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;61(18):1935-44.
  27. Gowda RM, Khan IA, Mehta NJ, Vasavada BC, Sacchi TJ. Cardiac arrhythmias in pregnancy: clinical and therapeutic considerations. Int J Cardiol 2003;88(2):129-33.
  28. Meregalli PG, Westendorp IC, Tan HL, Elsman P, Kok WE, Wilde AA. Pregnancy and the risk of torsades de pointes in congenital long-QT syndrome.
    Neth Heart J. 2008; 16(12):422-5.
  29. Seth R, Moss AJ, McNitt S, Zareba W, Andrews ML, Qi M, Robinson JL, Goldenberg I, Ackerman MJ, Benhorin J, Kaufman ES. Long QT syndrome and pregnancy. J Am Coll Cardiol. 2007; 49(10):1092-8.

ED Management of Heart Failure: Pearls & Pitfalls

Authors: Kristine Jeffers, MD (EM Resident at SAUSHEC) and Brit Long, MD (@long_brit, EM Attending Physician at SAUSHEC // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

 Case:

A 68-year-old male presented to the emergency department with chief complaint of dyspnea on exertion that had been worsening over the last week. Initial vitals were BP 120/100, HR 142, RR 22, T98.0, and Sat 96% on RA. An ECG obtained at triage is shown below.

screen-shot-2016-11-20-at-8-03-37-pm

On further questioning he reported general malaise over the last month and progressive dyspnea with exertion over the last week. He was no longer able to walk more than about 15 feet and used to care for his farm himself. He also reported significant swelling in his lower extremities that had been worsening over the last 4 days. He denied any medical problems or taking any medicines but had not been to a physician in over 20 years.

On physical exam, he was tachycardic with an irregularly irregular rhythm and no murmurs rubs or gallops, his lungs had crackles bilaterally, and he was mildly tachypneic. His abdomen was soft and nontender. His lower extremities had 2+ pitting edema to above the knees, and his pules were 2+ distally.

A portable CXR showed:

screen-shot-2016-11-20-at-8-03-49-pm

The patient’s symptoms were thought to be secondary to atrial fibrillation with rapid ventricular response. Due to his apparent fluid overload and unknown ejection fraction (EF), the patient was given 5mg of Metoprolol IV. This brought his heart rate down to 100-110. He was loaded with 100mg PO metoprolol at that time.

About 45 minutes after his heart rate had slowed, the patient appeared to be becoming more uncomfortable. He developed mild respiratory distress and became hypotensive. He was placed on BIPAP, and his blood pressure dropped to 55/24. At this time his extremities had become cool, and he was altered and agitated. A quick bedside ECHO showed diffuse hypokinesis. A central line and arterial line were placed, while push dose epinephrine was given to maintain perfusion.  Once the central line was in place, he was started on a dobutamine at 10mcg/kg/min and norepinephrine. At this time cardiology recommended emergent cardioversion, as the patient was persistently in atrial fibrillation (rate 110-120) with hypotension. He was given a small dose (40mg) of propofol and cardioverted with 200J with successful return to NSR. At that time he was transferred to the ICU for further care. 

Background

Acute heart failure (AHF) is a disease characterized by inadequate blood flow to meet metabolic demands. It often includes rapid onset of symptoms and signs secondary to abnormal cardiac function.1 AHF is a disease associated with high morbidity and mortality. It accounts for over 650,000 emergency department (ED) visits annually, with over 80% leading to admission.2 Those hospitalized are at high risk, with over one third of patients dying or requiring repeat admission within 90 days. In addition to the high burden of disease, AHF poses significant costs to the health system with over $39 billion per year.3

Pathophysiology

CHF ultimately develops from cardiac dysfunction, which leads to decreased cardiac output from myocardial stress or injury.  Anything that threatens cardiac output triggers a cascade activating the renin-angiotensin-aldosterone and sympathetic nervous systems. This leads to increased levels of norepinephrine, vasopressin, endothelin, and TNF-alpha, which result in sodium and water retention. This further increases systemic vascular resistance, cardiac workload, wall tension, and O2 demand. Over the long term this leads to cardiac remodeling, contributing to the cycle of congestive heart failure.3

screen-shot-2016-11-20-at-8-04-26-pm

Diagnosis

The diagnosis of ACHF is based on symptoms and clinical findings supported by appropriate investigations. Possible tests include ECG, CXR, electrolytes, liver function, biomarkers, and echocardiogram. Early diagnosis and initiation of treatment improves outcome.2 The following are suggestive of heart failure:

-History:  Dyspnea, orthopnea, fatigue, weakness, leg swelling, and abdominal swelling.6

-Physical Exam: Respiratory distress, rales, S3, JVD, hepatojugular reflux, hepatomegaly, ascites, edema, diaphoresis, tachycardia, hypoxia.4

-ECG: Often abnormal in heart failure. Identify the rhythm and assess for ACS, signs of strain, and dysrhythmia.

-CXR: Look for pulmonary congestion, effusions, and cardiomegaly. Also assess for focal consolidation or pneumothorax, which are other causes of dyspnea. Keep in mind that up to 20% of patients have no signs of congestion on CXR.2

Below is a summary of diagnostic accuracy of findings on chest radiograph and ECG for AHF in ED patients presenting with dyspnea.7

screen-shot-2016-11-20-at-8-04-47-pm

-Laboratory evaluations: VBG (pH, lactate), CBC, UA, electrolytes, LFTs, BNP, and troponin.

-BNP: This biomarker is a peptide released from cardiac ventricles in response to increased wall stretch and volume overload. During flash pulmonary edema levels may be normal, as rapid overload is not reflected by BNP elevation. It is also affected by renal failure, older age, female gender, and sepsis (all which increase BNP). Obesity can lower BNP levels. BNP demonstrates a strong predictive value of 90-day outcomes and correlation with in-hospital mortality as BNP worsens.2,6-8,20

-2007 AHFS Guidelines from ACEP recommend at level B obtaining a BNP or pro-BNP, which can improve diagnostic accuracy.22 It is also recommended as a class I recommendation by ACCF/AHA and JFSA guidelines where there is an uncertainty of the diagnosis.

ACEP recommends the following:  BNP <100 pg/dL or NT-proBNP <300 pg/dL suggests a diagnosis other than acute heart failure syndrome, while a BNP >500 pg/dL or NT-proBNP >1,000 pg/dL suggests acute heart failure syndrome.22

– Ultrasound: 3+ B-lines in one viewing field (from water-thickened interlobular septa at pleural line) can be used to diagnose pulmonary edema with varying sensitivity and specificity. Classically unilateral symptoms are more suggestive of pneumonia, while bilateral symptoms are thought to be cardiogenic.2 A review of recent literature on this subject with anywhere from novice users to US trained emergency physicians demonstrates 87-94% sensitivity and 49-92% specificity for the diagnosis of acute heart failure.8-14,21 Investigators also found improved accuracy when ultrasound was added to the history and physical exam, compared to gestalt alone.8-14,21

-Echo: assess EF, wall motion, IVC, and lung zones (b-lines).1

 Classification:

Patients presenting in heart failure can be placed into four basic categories based on their level of congestion and their level of perfusion. As seen below in the diagram, patients can present from dry and warm (normal) to cold and wet (cardiogenic shock). Patients presenting in the warm and wet category are the most common, but patients can present in shock without being fluid overloaded. Therapy must be tailored to where a patient falls on the spectrum below.4,5

screen-shot-2016-11-20-at-8-04-59-pm

 

Warm and Wet: AHF and Acute Pulmonary Edema

Acute Congestive Heart Failure Exacerbation

This is one of the most common types of CHF encountered in the emergency department. These patients present with a more indolent course, endorsing weight gain, edema, and dyspnea that worsens over days to weeks.1, 5 These patients may have reduced EF and history of CAD.2 These patients should be evaluated as discussed above, but the mainstay of acute treatment for them is diuresis.
Per the ACEP policy on AFH released in 2007 in which initiation of diuretics in the emergency department is addressed, there is a Class C recommendation that diuretics should be administered judiciously given the potential association of diuretics and worsening renal function at index hospitalization, which affects long-term mortality.22

Acute Pulmonary Edema

Patients may present in acute pulmonary edema, hypertension, and respiratory distress when their symptoms suddenly worsen. An increased screen-shot-2016-11-20-at-8-05-22-pmafterload often from elevated vascular pressures leads to hydrostatic lung edema as is seen in the images with initial presentation on the left and resolving fluid on the right.15 These patient present with respiratory distress, tachypnea, rales, crackles, orthopnea, and hypoxia. They are usually hypertensive.

Treatment for pulmonary edema focuses on preload and afterload reduction, followed by diuresis. Vasodilators are the mainstay for treating and relieving symptoms.19 Contraindications for vasodilators include flow limiting preload dependent states like RV infarct, aortic stenosis, or HOCM.

The 2007 emergency medicine practice guidelines also address diuretics, vasodilators, and noninvasive positive pressure ventilation.26

  • Vasodilators: There is a level B recommendation to treat patients presenting in AHF with associated dyspnea with IV nitrates. They have a level C recommendation that recommends nitroglycerin over nesiritide, as there is no clear evidence that nesiritide is superior. They state nesiritide should not be considered first line therapy. They also state that ACE inhibitors may be useful in the initial management of acute heart failure, but patients must be monitored for hypotension from the first dose.26
  • Nitroglycerin can be given sublingual or IV. Sublingual is useful while setting up a drip and delivers 400mcg over 5 minutes (close to 60-80mcg per minute). A nitroglycerin IV bolus can be given for hypertensive patients, ranging from 100 micrograms to 1mg, often dependent on the provider and institution. A drip should then be started and rapidly increased to reduce preload and afterload. This medication is essential for this category.
  • Nitroprusside is only given in a drip form. Nitroprusside should be started at 0.3mcg/kg/min IV and can be titrated up to 5 mcg/kg/minute. However, nitroglycerin properly dosed should improve blood pressure.
  • Nicardipine has been shown to increase cardiac output and decrease pulmonary artery pressures, leading to increased cardiac index. Doses used were 1-3 mcg/kg/min IV. Nicardipine may be effective as a potent vasodilator in the initial management of acute heart failure but should not be continued long term due to its effect on the renin-aldosterone-angiotensin system. Further study is warranted for nicardipine use in HTN heart failure.27
  • Diuretics: There is a level B recommendation to treat patients with moderate-to-severe pulmonary edema resulting from AHF with furosemide in combination with nitrate therapy. They also have a level C recommendation that monotherapy with diuretics in this setting is unlikely to prevent the need for endotracheal intubation, as opposed to monotherapy with nitrates.22 If the patient is hypertensive with pulmonary edema, use nitroglycerin first to improve fluid distribution and pulmonary edema, followed by diuretics after.

The initial starting dose for furosemide/Lasix varies in the literature, but most recommend initial dosing equal to the home dose in IV form, or 20mg IV for those who are furosemide naive.

– Noninvasive positive pressure ventilation: The level B recommendation is to use 5-10mmHg of CPAP for dyspneic patients with AHF without hypotension or the need for emergent intubation to improve heart rate, respiratory rate, blood pressure, and reduce the need for intubation. This treatment can reduce in-hospital mortality. The level C recommendation states BiPAP could also be considered as an alternative to CPAP.1-3,7,19

Cold and Wet: Cardiogenic Shock

Cardiogenic shock is an acute state of decreased cardiac output, resulting in inadequate tissue perfusion despite adequate or excessive circulating volume. This represents only a small subset of patients presenting in AHF (6-8%) but has a 50% mortality rate (half of those occur in the first 48 hours from diagnosis).1,5,16

Risk factors include massive MI (#1 cause), acute mitral regurgitation, VSD, free wall rupture, RV infarct, sepsis, myocarditis, cardiomyopathy, cardiac contusion, aortic stenosis, HOCM, mitral stenosis, myxoma, tamponade, and chordae rupture.16

The pathophysiology is poorly understood and variable based on the cause of shock. In post myocardial infarction it is thought that a release of inflammatory mediators like cytokines and nitric oxide synthase leads to high levels of nitric oxide. This in turn inhibits contractility, produces a decreased response to catecholamines, and induces vasodilation.

Physical examination will reveal signs of hypoperfusion. The patient may exhibit altered mental status, decreased urine output, systolic blood pressure <90 mmHg, a narrowed pulse pressure of <20, tachycardia, tachypnea, rales, JVD, hepatojugular reflex, peripheral edema, diaphoresis, or a new heart murmur.

The diagnosis is largely clinical based on signs of poor cardiac output and tissue hypoperfusion in addition to signs of fluid overload.

The treatment of cardiogenic shock in the emergency department focuses on temporizing measures until more definitive management correcting the inciting event can occur (surgery, cath lab/PCI…).

-Airway: There is no need to withhold O2 from these patients. Supplemental oxygen, NIPPV, or intubation may be required to maintain adequate oxygenation pending respiratory failure. Preoxygenation is essential for these patients, so start supplemental oxygen right away. Have low threshold to start NIPPV, which can rapidly improve these patients. One thing to consider first is that positive pressure from intubation, which further decreases preload and cardiac output, can worsen hypotension. Be prepared with fluids, pressors, and inotropes if intubation is needed.

-Stabilization: Go back to the basics… Establish your safety net of IV access, supplemental oxygen, and monitors. Consider invasive monitoring with central line and arterial line. Patients may even benefit specific therapies including intra-aortic balloon pump or early PCI, so get your consultants on board early!1,16

-Hypotension: Treatment should be guided by clinical findings. Your decision for fluids vs inotropes (dobutamine) vs pressors (norepinephrine) should be guided by clinical findings.1,16 In those with hypotension, norepinephrine should be started. Once blood pressure stabilizes, then dobutamine can be added.

Cold and Dry

Patients presenting in a low cardiac output state without fluid overload are rare and surprisingly stable clinically. They do not often present with acute symptoms. Adjustments to oral medications are not helpful unless there are problems with filling pressure or excessive vasodilation. Use caution in starting inotropes, as these patients may become dependent or develop tachyphylaxis.5 Beta-blockers if tolerated are associated with later clinical improvement, but there is little evidence and few trials focusing on this group.5 These patients will require cardiology consultation and likely inpatient admission.

Risks of poor outcome

Risks of poor outcome in patients with acute decompensated heart failure include a history of prior hospitalization, markedly elevated BNP (>1000 pg/ml), sodium <136mmol/L, BUN >43mg/dl,  SPB <115, or positive troponin. Admission to a critical care unit may be needed for these patients.

In the setting of AHF, SBP demonstrates a differential prognostic association with mortality according to LVEF status. When EF is <40%, SBP is inversely and linearly associated with mortality, whereas patients with a LVEF 50% demonstrate a J-curve pattern, with the lowest risk being in the SBP category 160–179 mmHg and a progressive increased risk of mortality above and below these values.17

Disposition


Over 80% of patients with acute heart failure will be admitted to the hospital. There are few recommendations and no national guidelines outlining who may be appropriate for discharge. Determining who is high versus low risk is difficult, and many of these patients are at high risk of mortality.20,23,25

The Ottawa heart failure risk scale is one such tool that has been proposed. It is based on a retrospective analysis of patients seen in the ED with heart failure. The goal of the score is to identify patients at high risk of serious adverse outcomes (SAE). The score uses 10 pieces of data, worth up to 15 points. Components of the history, screen-shot-2016-11-22-at-7-32-22-amphysical, and lab results are used. Patients who score 0 are considered low risk of adverse outcome, with 2.8% risk of SAE. Depending on the cutoff used for admission, whether 0, 1, or 2 points, admission rates can be reduced. By using a score of 2 for admission, you maintain an 80% sensitivity for SAE and would admit approximately 50% of patients, as opposed to the current average in the United States (close to 80% of patients).

Several papers have been published investigating decision tools to decide who is high and who is low risk and appropriate for discharge. The problem with many of these tools is they are retrospectively based, and very few have been externally validated.7,8  More work needs to be done to evaluate low risk heart failure patients in the ED. One possible way to utilize a scoring tool would be to use them in combination with an observation unit.

Some have recommended a short course in the ED or even an ED-based observation unit where many of the chronic (but worsened and overloaded) patients could be managed without full admission.18,24 These observation units have the possibility of reducing cost and admission rates, and many ED physicians are knowledgeable in the initial management of acute heart failure syndrome. Many of the factors of inpatient versus outpatient management are based on the individual and the institution. It will require a collaboration of both inpatient and outpatient care to provide comprehensive treatment for these patients.25 Early follow up for these patients has been shown to have a positive impact on 30-day readmission rates, reinforces medication compliance, and allows for patient education.6,7

Pharmacotherapy

A variety of agents have been mentioned in this post that are available for management of these patients.  A summary of the dose and mechanism of action of these medications is shown below, as well as their site of action.

Diuretics Medication Dose Mechanism Other
Lasix/furosemide IV >/= to home dose of oral Inhibits Na/Cl reabsorption in the loop of Henle Ototoxicity, hyperuricemia, hyperglycemia
Bumetanide 0.5-2 mg/dose (max10mg/day) 40x more potent than lasix
Torsemide 10-20mg Q2H
Vasodilators Nitroglycerin 20-200mcg/minute Relieves pulmonary congestion. Reduces preload and afterload without impairing tissue Perfusion Headache, methemoglobinemia with high doses
Nitroprusside 0.3 mcg/kg/min and up causes cyanide toxicity, hypotension
Inotropes Dopamine <2 mcg/kg/min Dopaminergic receptors. Used for hypoperfusion unresponsive to other therapies. Increases contractility
>2 mcg/kg/min Beta receptor agonist
>5 mcg/kg/min Alpha receptor agonist
Dobutamine 2-20 mcg/kg/min up to 40 mcg/kg/min Beta receptor agonist  Initial choice in cardiogenic shock. If on beta blocker may need high doses to restore inotropic effect.
PDE Inhibitors Milrinone 25 mcg/kg bolus then 0.375-0.75 mcg/kg/min Type III phosphodiesterase inhibitor alternative agent in cardiogenic shock refractory to other agents
Vasopressors Epinephrine 1mcg/min up to 35 mcg/min Catecholamine, alpha and beta receptors Pressor of choice in anaphylactic shock. 2nd choice after norepi
Norepinephrine 2-4 mcg/min up to 100mcg/min Alpha and beta adrenergic Vasopressor of choice in septic, cardiogenic and hypovolemic shock
Phenylephrine 20-80 mcg/min up to 360mcg/min Alpha adrenergic Initial pressor when limited by tachycardia, Decreases stroke volume and cardiac output
Cardiac Glycosides Digitalis 0.125-0.25mg Inhibits Na/K ATPase-> increases intracellular Ca Indicated if LV dysfunction with continued NYHA-FC II, III, or IV symptoms

Summary

Congestion will be absent from chest x-rays about 20% of the time… don’t be fooled. Bedside US can really benefit, and BNP may be used to help confirm the diagnosis in these patients.

-Ultrasound is a great new addition to confirming the diagnosis of AHF.

-The vast majority of patient presenting with AHF fall into the warm and wet category. Mainstay of treatment for these patients is diuresis. Start with their home dose of Furosemide/Lasix IV.

-Patients presenting in acute pulmonary edema are going to respond best to vasodilators (nitrates), as diuretics will have little effect acutely.

BiPAP or CPAP should be used in the dyspneic patient.

-Cardiogenic shock is rare but life threatening: Remember your ABCs.

-Positive pressure from intubation further decreases preload and cardiac output which can worsen hypotension. Be prepared to counteract this (push dose epi… norepinephrine… dobutamine).

-Dobutamine is first choice for low cardiac output.

-Norepinephrine is the first choice vasopressor.

 

References/Further Reading

  1. Nieminen M, Bohm M, Cowie M, et al. Executive summary of the guidelines on the diagnosis and treatment of acute heart failure. Eur Heart J. 2005;26:384-416.
  2. Peacock WF, Cannon CM, Singer AJ, Hiestand BC. Considerations for initial therapy in the treatment of acute heart failure. Crit Care. 2015;19(399). doi:10.1186/s13054-015-1114-3.
  3. Peacock WF. Congestive Heart Failure and Acute Pulmonary Edema. In: Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, Seventh Edition. ; 2011:405-415.
  4. Thomas SS, Nohria A. Hemodynamic classifications of Acute Heart Failure and their Clinical Application. Circ J. 2012;76:278-286.
  5. Nohria A, Lewis E, Stevenson LW. Medical Management of Advanced Heart Failure. J Am Med Assoc. 2002;287(5):628-640.
  6. Fermann GJ, Collins SP. Initial Management of Patients with Acute Heart Failure. Heart Fail Clin. 2013;9(3):291-306. doi:10.1016/j.hfc.2013.04.004.
  7. Collins SP, Storrow AB, Levy PD, et al. Early Management of Patients With Acute Heart Failure: State of the Art and Future Directions: A Consensus Document from the SAEM/HFSA Acute Heart Failure Working Group. Acad Emerg Med. 2015;22(1):94-112. doi:10.1111/acem.12538.
  8. Otterness K, Milne WK, Carpenter CR. Hot off the Press: B-lines and Focused Lung Ultrasound to Diagnose Acute Heart Failure in Dyspneic Patients. Acad Emerg Med. 2015;22(9):1122-1124. doi:10.1111/acem.12751.
  9. Liteplo AS, Marill KA, Villen T, et al. Emergency thoracic ultrasound in the differentiation of the etiology of shortness of breath (ETUDES): Sonographic B-lines and N-terminal Pro-brain-type natriuretic peptide in diagnosing congestive heart failure. Acad Emerg Med. 2009;16(3):201-210. doi:10.1111/j.1553-2712.2008.00347.x.
  10. Vitturi N, Soattin M, Allemand E, Simoni F, Realdi G. Thoracic ultrasonography: A new method for the work-up of patients with dyspnea. J Ultrasound. 2011;14(3):147-151. doi:10.1016/j.jus.2011.06.009.
  11. Pirozzi C, Numis FG, Pagano A, Melillo P, Copetti R, Schiraldi F. Immediate versus delayed integrated point-of-care-ultrasonography to manage acute dyspnea in the emergency department. Crit Ultrasound J. 2014;6(1):5. doi:10.1186/2036-7902-6-5.
  12. Mantuani D, Frazee BW, Fahimi J, Nagdev A. Point-of-Care Multi-Organ Ultrasound Improves Diagnostic Accuracy in Adults Presenting to the Emergency Department with Acute Dyspnea. West J Emerg Med. 2016;17(1):46-53. doi:10.5811/westjem.2015.11.28525.
  13. Gallard E, Redonnet JP, Bourcier JE, et al. Diagnostic performance of cardiopulmonary ultrasound performed by the emergency physician in the management of acute dyspnea. Am J Emerg Med. 2015;33(3):352-358. doi:10.1016/j.ajem.2014.12.003.
  14. Al Deeb M, Barbic S, Featherstone R, Dankoff J, Barbic D. Point-of-care ultrasonography for the diagnosis of acute cardiogenic pulmonary edema in patients presenting with acute dyspnea: a systematic review and meta-analysis. Acad Emerg Med. 2014;21(8):843-852. doi:10.1111/acem.12435.
  15. Matthay MA. Resolution of pulmonary edema thirty years of progress. Am J Respir Crit Care Med. 2014;189(11):1301-1308. doi:10.1164/rccm.201403-0535OE.
  16. Weber JE, W. Frank Peacock. Cardiogenic Shock. In: Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, Seventh Edition. ; 2011:385-389.
  17. Nunez J, Nunez E, Fonarow GC, et al. Differential prognostic effect of systolic blood pressure on mortality according to left-ventricular function in patients with acute heart failure. Eur J Heart Fail. 2010;12:38-44. doi:10.1093/eurjhf/hfp176.
  18. Weintraub NL, Collins SP, Pang PS, et al. Acute Heart Failure Syndromes: Emergency Department Presentation, Treatment, and Disposition: Current Approaches and Future Aims: A Scientific Statement from the American Heart Association. 2010. doi:10.1161/CIR.0b013e3181f9a223.
  19. Fenwick R. Management of acute heart failure in the emergency department. Emerg Nurse. 2015;23(8):26-35.
  20. Cohen-Solal A, Laribi S, Ishihara S, et al. Prognostic markers of acute decompensated heart failure: The emerging roles of cardiac biomarkers and prognostic scores. Arch Cardiovasc Dis. 2015;108:64-74. doi:10.1016/j.acvd.2014.10.002.
  21. Rempell JS, Noble VE. Using lung ultrasound to differentiate patients in acute dyspnea in the prehospital emergency setting. Crit Care. 2011;15(3):161. doi:10.1186/cc10226.
  22. Silvers SM, Howell JM, Kosowsky JM, Rokos IC, Jagoda AS. Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department with Acute Heart Failure Syndromes. Ann Emerg Med. 2007;49(5):627-669. doi:10.1016/j.annemergmed.2006.10.024.
  23. Collins S, Hiestand B. Confounded by hospitalization: risk stratification and admission decisions in emergency department patients with acute heart failure. Acad Emerg Med. 2013;20(1):106-107. doi:10.1111/acem.12045.
  24. Schrock JW, Emerman CL. Observation Unit Management of Acute Decompensated Heart Failure. Heart Fail Clin. 2009;5(1):85-100. doi:10.1016/j.hfc.2008.08.015.
  25. Collins SP, Storrow AB. Acute Heart Failure Risk Stratification: Can We Define Low Risk? Heart Fail Clin. 2009;5(1):75-83. doi:10.1016/j.hfc.2008.08.010.
  26. Stiell IG, Clement CM, Brison RJ, et al. A risk scoring system to identify emergency department patients with heart failure at high risk for serious adverse events. Acad Emerg Med. 2013;20(1):17-26. doi:10.1111/acem.12056.
  27. McFarland, Scott and Silvers S. Clinical Policy: Management of Acute Heart Failure Syndromes. ACEP News. https://www.acep.org/Clinical—Practice-Management/Clinical-Policy–Management-of-Acute-Heart-Failure-Syndromes/. Published 2007. Accessed February 11, 2016.
  28. Curran MP, Robinson DM, Keating GM. Intravenous Nicardipine Its Use in the Short-Term Treatment of Hypertension and Various Other Indications. Drugs. 2006;66(13):1755-1782.

R.E.B.E.L. EM – Beyond ACLS: Pre-Charging the Defibrillator

Originally published at R.E.B.E.L. EM on March 24, 2016. Reposted with permission.

Follow Dr. Salim R. Rezaie at @srrezaie and Sam Ghali at @EM_RESUS

Post Written By: Sam Ghali (Twitter: @EM_RESUS)

Beyond ACLS - Pre-Charging the DefibrillatorIn cardiac arrest care there has been a lot of focus over the years on limiting interruptions in chest compressions during CPR. In fact, this concept has become a major focus of the current AHA Guidelines. Why? Because we know interruptions are bad [1,2]. One particular aspect of CPR that has gotten a lot of attention in this regard is the peri-shock period. It has been well established that longer pre- and peri-shock pauses are independently associated with decreased chance of survival [3,4].

Traditionally when a shockable rhythm is encountered at the rhythm check, providers will charge the uncharged defibrillator at that time. In the meantime, chest compressions are typically resumed while waiting for the defibrillator to charge. Once the defibrillator has finished charging, providers are then forced to pause yet again in order to deliver the shock.

Realizing the vital importance of minimizing pauses in chest compressions, it has recently become popular for providers to go as far as continuing to perform chest compressions during defibrillation (“hands-on defibrillation”) – the goal being to effectively eliminate the additional interruption. There has been much debate as to whether this practice is safe for the provider or not. I am not going to get into this debate here as it has already been discussed on REBEL EM.

Instead, I would like to focus on what I believe to be a simple maneuver that based on existing evidence and simple logic should be implemented as standard care: 

Pre-charging the defibrillator during the active chest compression phase of CPR, in anticipation of a shockable rhythm at the rhythm check.

Why should we wait until a shockable rhythm is encountered at the rhythm check to charge the defibrillator? This makes very little sense. Charging the defibrillator prior to the rhythm check is far more logical. With the defibrillator already charged and ready to go, if a shockable rhythm is encountered at rhythm check, the shock can be delivered immediately without any delay and importantly – a second interruption can be averted entirely.

So why has an illogical sequence of events become standard care in CPR? The answer is simple: it’s because that’s the way CPR has always been taught per ACLS. From the 2010 AHA/ACC guidelines:  

“When a rhythm check by a manual defibrillator reveals VF/VT, the first provider should resume CPR while the second provider charges the defibrillator. Once the defibrillator is charged, CPR is paused to ‘clear’ the patient for shock delivery. After the patient is ‘clear,’ the second provider gives a single shock as quickly as possible to minimize the interruption in chest compressions (‘hands-off interval’).”

                 This is how this plays out during CPR: 

2 Pauses

CPR WITHOUT PRE-CHARGE

Image Modified from [2] The exact decrease in perfusion pressure for a specific time period is obviously variable, but this pictorial gives you an idea of the sequence of events and highlights the delay in shock delivery and the resulting detriment in not just one, but two interruptions in chest compressions.

By pre-charging the defibrillator during the active chest compression phase of CPR, encountering a shockable rhythm at the rhythm check plays out like this:

1 Pause

CPR WITH PRE-CHARGE FINAL

Image Modified from [2] Note: not only is the shock delivered earlier but the second interruption is avoided completely.

If the rhythm check happens to reveal a non-shockable rhythm, CPR can continue as per usual without any alteration. Of note, current defibrillators will “hold” the shock for some time (~60 seconds), and if the shock is not delivered in this time frame, the charge will dissipate and require re-charging. Therefore pre-charging should take place within this set time frame prior to a rhythm check. (Simply test your particular defibrillator to figure out exactly how long it holds the charge).

The only arguments I have ever heard against the implementation of this strategy is that it may increase the incidence of inappropriate or inadvertent shocks. The only study I know of looking at this method was a multi-center retrospective study from 2010 from Edelson et al [5]. Data were gathered from CPR-sensing defibrillator transcripts over a 3-year period. They looked at a total of 680 charge-cycles from 244 cardiac arrests. There was no difference in inappropriate shocks and there was only one instance of inadvertent shock administration during compressions (which went unnoticed by the compressor).

There will likely never be robust data looking at this particular aspect of CPR. It’s a small thing, but with potentially huge impact. I have personally been practicing CPR this way for years now. It has been my experience that it is an incredibly smooth process. All it takes is a little practice and team de-briefing to ensure all providers are on the same page. Does it improve outcomes? We may never definitively know. Will it ever make the guidelines? I suspect that eventually it will, perhaps with verbiage similar to something like this:

“It is reasonable to consider pre-charging the defibrillator during chest compressions…”

 Until then, it is my opinion that based on data we do have, logic, and reasoning that pre-charging the defibrillator in anticipation of a shockable rhythm at the rhythm check is how we should be running our codes.

Clinical Bottom Line: Pre-charging the defibrillator during chest compressions in anticipation of a shockable rhythm at the rhythm check, decreases time to defibrillation and minimizes the number of pauses in chest compressions during CPR.

References:

  1. Berg RA et al. Adverse hemodynamic effects of interrupting chest compressions for rescue breathing during cardiopulmonary resuscitation for ventricular fibrillation cardiac arrest. Circulation 2001; 104 (20): 2465 – 70. PMID: 11705826.
  2. Cunningham LM et al. Cardiopulmonary resuscitation for cardiac arrest: the importance of uninterrupted chest compressions in cardiac arrest resuscitation. Am J Emerg Med 2012; 30 (8): 1630 – 8. PMID: 22633716
  3. Brouwer TF et al. Association Between Chest Compression Interruptions and Clinical Outcomes of Ventricular Fibrillation Out-of-Hospital Cardiac Arrest. Circulation 2015;132(11):1030-7. PMID: 26253757 
  4. Cheskes S et al. Perishock pause: an independent predictor of survival from out-of-hospital shockable cardiac arrest. Circulation 2011; 124 (1): 58 – 66. PMID: 21690495
  5. Edelson DP et al. Safety and efficacy of defibrillator charging during ongoing chest compressions: a multi-center study.  Resuscitation 2010; 81(11):1521-6. PMID: 20807672 

Post Peer Reviewed By: Salim R. Rezaie (Twitter: @srrezaie) and Anand Swaminathan (Twitter: @EMSwami)

An Approach to Bradycardia in the Emergency Department

Authors: Patrick C Ng, MD (EM Chief Resident, SAUSHEC Emergency Medicine Department) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC Emergency Medicine Department) // Edited by: Jennifer Robertson, MD, MSEd and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW Medical Center / Parkland Memorial Hospital)

 Case

A 15-year-old male is brought to the emergency department (ED) via ambulance with a chief complaint of syncope. He reports that he was washing his hands in the bathroom at approximately 4:00 AM and the next thing he remembers, he was waking up to paramedics putting him on a stretcher. He denies preceding symptoms and does not report any relieving or exacerbating features. This has never happened to him before.

His review of systems is positive for recent rhinorrhea, cough, mild chest discomfort, and a low grade fever. His primary care physician was treating him symptomatically with a working diagnosis of an upper respiratory infection. The patient states that his symptoms had been improving.

Emergency medical services (EMS) reports the following vital signs on scene: blood pressure of 70/40 mm Hg, a heart rate of 36 beats per minute (bpm), a respiratory rate (RR) of 16/minute, a temperature of 100.6°Fahrenheit (F), an oxygen saturation of 98% on room air (RA), and a glucose level of 120. The patient’s vital signs upon arrival to your ED were similar and did not change despite intravenous (IV) fluids. A STAT echocardiogram was ordered and revealed decreased cardiac function. Laboratory tests were significant for an elevated troponin and white blood cell (WBC) count. A respiratory viral panel is positive for Coxsackie virus.

The patient’s electrocardiogram (EKG) is as follows:

pic1

(Image reproduced from: http://www.revespcardiol.org/; last accessed 10/19/2016)

You place pacing pads on the patient and start him on a dobutamine drip. He gets admitted to the pediatric intensive care unit and receives IV immunoglobulin (IVIG) for 3 days. He is downgraded to the floor and is discharged a week later with a discharge diagnosis of bradycardia and sick sinus syndrome, likely secondary to viral myocarditis.

This article will evaluate the ED approach to bradycardia. Before we get to the evaluation and management of the sick bradycardic patient, a little background in conduction is necessary…

Introduction

The cardiac conduction system consists of the His-Purkinje system. Electrical impulses are generated in the sinoatrial (SA) node, conducted down to the atrioventricular (AV) node, and then conducted down to the ventricles via the left and right bundle branches (Figure 1). A normal heart rate is typically between 60-100 bpm. Bradycardia is defined according to some sources as a heart rate below 60 bpm1.

pic2

Figure 1: Electrical conduction system of the heart. Image reproduced from: (http://1.bp.blogspot.com/-SfYtiDdSvC8/Tw2HuHJZ3ZI/AAAAAAAAALM/xkXHDdlt_Wk/s1600/conduction+system+of+the+heart.png) – Last Accessed 10/19/2016.

Bradycardia can be organized into two main categories: symptomatic and asymptomatic. Bradycardia can be normal in various individuals, particularly in children and well-conditioned athletes2,3. Some reports describe asymptomatic individuals with profound bradycardia defined as a HR <35 bpm. Findings of bradycardia in these individuals may not require any intervention, as long as the patient does not experience symptoms.

This is the opposite of patients with symptomatic bradycardia. The signs and symptoms of bradycardia are not specific and may include syncope, dizziness, chest pain, shortness of breath, and fatigue4. A slow heart rate can lead to heart failure and/or hemodynamic instability 5. Upon initial presentation, it is imperative the ED provider focus the history on determining if the patient is symptomatic.

The differential for symptomatic bradycardia is broad. One way to look at the differential is by broad categories which includes but is not limited to: structural/electrophysiological, infectious, endocrine, toxicology/iatrogenic, and other (Table 1).

Table 1 – Etiologies of Bradycardia

Category Possible Etiologies
Structural/Electrophysiological -Sick Sinus Syndrome

-AV Block

-Ischemia

-Congenital Heart Disease

-Prior Cardiac Surgery

-Cardiomyopathy

-Arterial Dissection (Aorta, Coronary, Carotid)

Infectious -Myocarditis

-Lyme Disease

-Bunyavirus

-Dengue*

-Typhoid Fever*

-Legionnaires disease*

-Psittacosis*

-Leptospirosis*

-Malaria*

-Babesiosis*

-Q fever*

-Yellow Fever*

-Rocky Mountain Spotted Fever*

Endocrine -Hypothyroidism/Myxedema coma

-Bamforth syndrome

-Hypothalamic dysfunction

-Electrolyte Abnormalities/Malnutrition

-Hashimoto’s thyroiditis

Toxicology/Iatrogenic -Beta blocker**

-Calcium channel blocker**

-Clonidine**

-Guanfacine**

-Digoxin**

-Lidocaine**

-Donepezil**

-Organophosphate poisoning

-Tacrine

-Carbamate insecticide poisoning

-Opioid**

-Tricyclic Antidepressant Poisoning

-Midodrine**

-Levetiracetam overdose

-Amitraz

Other -Heat exhaustion/stroke

-Hypothermia

-Leukomalacia

-Increased Intracranial Pressure

-Spinal Cord Injury

-Carotid hypersensitivity syndrome

-Chromosome 19p duplication syndrome

-Fleisher syndrome

-Young Simpson syndrome

-Asphyxia neonatorum

-Pneumothorax

-Lupus Carditis

-Oculocardiac Reflex

-Dexmedetomidine

-Prostaglandin

Table 1: Causes of bradycardia8-20 (Not an all-inclusive list)

*Can cause relative bradycardia i.e. not in proportion to fever

** In overdose, and also at therapeutic dose

What are the key ED studies?

An EKG should be one of the first diagnostic tests obtained when bradycardia is recognized. Additionally, depending on the suspected etiology, a troponin, brain natriuretic peptide (BNP), electrolytes, infectious labs, chest x-ray, neuroimaging, and echocardiogram should be considered.  The workup should be tailored to the initial clinical assessment. Not all patients warrant these tests.

The EKG is imperative, and examples of various heart blocks are shown below:

first-degree-b-lock

1st degree heart block- Image reproduced from: https://umem.org/files/uploads/content/ECG%20Challenge/Marked%201st%20degree%20AVB.jpg; last accessed 10/25/2016.

2nd-degree-block

2nd degree block-Type I, Image reproduced from: http://www.patientcareonline.com/sites/default/files/cl/1527433.png; last accessed 10/25/2016.

2nd-degree-block-type-2

2nd degree block-Type II, Image reproduced from: http://www.cardiocareconcepts.com/AV_Block_2.jpg; last accessed 10/25/2016

3rd-degree-block

3rd degree block Image reproduced from: http://1.bp.blogspot.com/-qDCMtbuI1Zk/VFLbhSrRI-I/AAAAAAAAFRA/TqIn_yXm54I/s1600/Bradycardia%2Bwide%2BQRS%2Bthird%2Bdegree%2Bheart%2Bblock.png; last accessed 10/25/2016.

one-after-the-3rd-degree-block-pic

Sick Sinus-Alternating patterns of tachy- and bradyarrhythmia which can be seen with sick sinus syndrome. Image reproduced from: http://www.aafp.org/afp/2003/0415/p1725.html; last accessed 10/25/2016.

Management

As mentioned in the introduction, not all bradycardic rhythms require intervention, especially in the otherwise healthy, asymptomatic patients. If the ED provider is presented with a patient with symptomatic bradycardia, one of the first things to consider is the placement of transcutaneous pacer pads. Preparation for transvenous pacing (which requires a central line) should also be considered. Specific discussion of management plans for the different etiologies listed in Table 1 is too lengthy and out the scope of this post. General categories are mentioned below.

Structural/Electrophysiological (EP): A general way to approach potential structural/EP causes of bradycardia is to consider an abnormality that hinders the normal conduction of the heart. To address this, the emergency provider should consider transcutaneous/transvenous pacing to temporize the patient until definitive treatment can be obtained, such as percutaneous coronary intervention (PCI) for a ST elevation myocardial infarction (STEMI) or a permanent pacemaker for conduction abnormalities.  An echocardiogram can assist in evaluation if a structural cause is suspected.

Infectious: Viral myocarditis is a more common cause of bradycardia in the infectious category. Myocarditis leading to hemodynamic compromise is important to consider, particular in the febrile, crashing child. Vasopressors, IVIG, and extracorporeal membrane oxygenation (ECMO) therapy have been reported in treating cardiogenic shock secondary to infectious etiologies. For further reading, consider reviewing: http://www.emdocs.net/pediatric-cardiogenic-shock/. Antibiotic therapy should be considered, particularly with tick-borne diseases such as Lyme disease.

Endocrine: Specific electrolyte and hormone abnormalities should be corrected. Thyroid disorders are a commonly reviewed topic for the emergency medicine inservice/board exam. For further management on myxedema coma, please review: http://www.emdocs.net/myxedema-aka-decompensated-hypothyroidism-an-em-primer/. An abnormal thyroid stimulating hormone can drastically change your management pathway. However, disorders such as thyrotoxicosis and myxedema coma are clinical diagnoses. The patient with myxedema coma should be given IV T4. IV T3 is an option as well, though it carries a higher risk of dysrhythmias.

Toxicology: The specific management plans for each potential toxin listed is out of the scope of this post. Beta blocker and calcium channel blocker toxicity is commonly seen in review books and examinations. Treatment includes glucagon, calcium supplementation, high dose insulin/glucose therapy, and potentially lipid emulsion therapy. For further reading on this topic, one can consider reviewing: http://www.emdocs.net/selected-toxicologic-bradycardias/

For cholinergic and hypnotic/sedative management, please review: http://www.emdocs.net/the-approach-to-the-poisoned-patient/

When reviewing medications and drug toxicity, it is vital to obtain a detailed medication reconciliation on patients with bradycardia, as a myriad of medications can cause a low heart rate.

Other: For etiologies listed in this category, there are a few management principles to consider for specific etiologies. For example, the emergency provider should understand the increased susceptibility of arrhythmias in the hypothermic patient.  Warming these patients should take precedence over other interventions such as introducing a transvenous pacer. This is because without warming, hardware can cause a deadly arrhythmia.

For neurogenic/traumatic etiologies of bradycardia such as head trauma, specific interventions to decrease intracranial pressure (ICP) (head elevation, mannitol, hyperventilation, 3% saline) should be considered.

Summary

As seen, the differential for bradycardia is broad, and management depends on the suspected etiology. Not all bradycardia can be fixed with atropine and pacing. The emergency provider must focus his or her history and physical to narrow the differential to address the underlying pathology to effectively treat symptomatic bradycardia.

Overall remember that: 

-Bradycardia is defined as a HR <60bpm

-Bradycardia can be benign and asymptomatic

-An EKG is essential to obtain as early as possible

-There is a broad differential for symptomatic bradycardia, and one can organize some of the causes into 5 categories: Structural/EP, Infectious, Endocrine, Toxicology/Iatrogenic, and Other

-Temporizing measures such as vasoactive drugs and pacing should be considered, but may not be effective in certain patients

References/Further Reading

  1. Spodick DH. Normal sinus heart rate: sinus tachycardia and sinus bradycardia redefined. Am Heart J. 1992 Oct;124(4):1119-21.
  2. Northcote RJ, Canning GP, Ballantyne D. Electrocardiographic findings in male veteran endurance athletes. Br Heart J. 1989 Feb; 61(2):155-60.
  3. Talan DA, Bauernfeind RA, Ashley WW, Kanakis C Jr, Rosen KM. Twenty-four hour continuous ECG recordings in long-distance runners. Chest 1982;82(1):19.
  4. Eraut D, Shaw DB. Sick sinus syndrome. Br Med J. 1973 Aug 4;3(5874):295.
  5. Tresch DD, Fleg JL. Unexplained sinus bradycardia: clinical significance and long-term prognosis in apparently healthy persons older than 40 years. Am J Cardiol. 1986 Nov 1;58(10):1009-13.
  6. Lateef A, Fisher DA, Tambyah PA. Dengue and Relative Bradycardia. Emerg Infec Dis. 2007 Apr;13(4):650-651.
  7. Ostergaard L, Huniche B, Andersen PL. Relative bradycardia in infectious diseases. J infect 1996;33:185-91.
  8. Tanriverdi S, Ulger Z, Siyah BB, Kultursay N, Yalaz M, Koroglu OA. Treatment of Congenital Complete Atrioventricular Heart Block With Permanent Epicardial Pacemaker in Neonatal Lupus Syndrome. Iran Red Crescent Med J. 2015 Sep 1;17(9):e16200
  9. Skog A, Lagnefeldt L, Conner P, Wahren-Herlenius M, Sonesson SE. Outcome in 212 anti-Ro/SSA-positive pregnancies and population-based incidence of congenital heart block. Acta Obstet Gynecol Scand. 2016 Jan;95(1):98-105.
  10. St-Onge M, Anseeuw K, Cantrell FL. Gilchrist IC, Hantson P, Bailey B, et al. Experts Consensus Recommendations for the Management of Calcium Channel Blocker Poisoning in Adults. Crit Care Med. 2016 Oct 3.
  11. Wong LY, Wong A, Robertson T, Burns K, Roberts M, Isbister GK. J Med Toxicol. 2016 Jul 4.
  12. Page CB, Mostafa A, Saiao A, Grice JE, Roberts MS, Isbister GK. Cardiovascular toxicity with levetiracetam overdose. Clin Toxicol. 2016;54(2):152-4.
  13. Roberts DM, Gallapatthy G, Dunuwille A, Chan BS. Pharmacological treatment of cardiac glycoside poisoning. Br J Clin Pharmacol. 2016 Mar;81(3):488-95.
  14. Dhooria S, Behera D, Agarwal R. Amitraz: a mimicker of organophosphate poisoning. BMJ Case Rep. 2015 Oct 1;2016.
  15. Graudins A, Lee HM, Druda D. Calcium channel antagonist and beta-blocker overdose: antidotes and adjunct therapies. Br J Clin Pharmacol. 2016 Mar;81(3):453-61.
  16. Leung AM. Thyroid Emergencies. J Infus Nurs. 2016 Sep-Oct;39(5):281-6.
  17. Wang FF, Xu L, Chen BX, Cui M, Zhang Y. Anorexia with sinus bradycardia: a case report. Beijing Da Xue Xue Bao. 2016 Feb 18;48(1):180-2.
  18. Alhussin W, Verklan MT. Complications of Long-Term Prostaglandin E1 Use in Newborns with Ductal-Dependent Critical Congenital Heart Disease. J Perinat Neonatal Nurs. 2016 Jan-Mar;30(1):73-9.
  19. Partida E, Mironets E, Hou S, Tom VJ. Cardiovascular dysfunction following spinal cord injury. Neural Regen Res. 2016 Feb;11(2):189-94.
  20. Thomsen JH, Nielsen N, Hassager C, Wanscher M, Pehrson S, Kober L, et al. Bradycardia During Targeted Temperature Management: An Early Marker of Lower Mortality and Favorable Neurologic Outcome in Comatose Out-of-Hospital Cardiac Arrest Patients. Crit Care Med. 2016 Jan;50(1):51-4.

R.E.B.E.L. EM – Is ST-Segment Elevation in Lead aVR Getting Too Much Respect? with Amal Mattu

Originally published at R.E.B.E.L. EM on March 4, 2016. Reposted with permission.

Follow Dr. Salim R. Rezaie at @srrezaie and Amal Mattu at @AmalMattu

Lead aVR is a commonly ignored lead and I have even heard of it avrreferred to as the Rodney Dangerfield of ECG leads as it gets no respect. I have anecdotally heard many EM physicians activate the cath lab for STE in lead aVR and many cardiologists say that these are not STEMI patients. So is lead aVR now getting too much respect? Well, I thought it would be a great idea to bring the great Amal Mattu on to the show to answer a few questions for us regarding STE in lead aVR.

If you don’t know Amal Mattu by now, I am not sure where you have been. Currently he is a tenured professor of Emergency Medicine at the University of Maryland School of Medicine in Baltimore. He has presented at numerous national and international conferences on ECG interpretation, published several books on the topic and if you want more from him just checkout his site ecgweekly.com

Is ST-Segment Elevation in Lead aVR Getting Too Much Respect? with Amal Mattu

Audio Player – Visit website to listen to Podcast

Click here for Direct Download of Podcast

Amal Mattu

Tenured Full Professor of Emergency Medicine
University of Maryland, Baltimore, MD
Twitter: @amalmattu
Blog: ecgweekly.com

Lets Start with a Historical Perspective on Troponin:

It was the mid 90’s when Troponin first got introduced into our clinical practice.  We already had CK , CK-MB, and myoglobin, but when Troponin got introduced, many felt it was 100% cardio-specific.  In other words, if Troponin was positive, it could only be due to a myocardial infarction.  But as Troponin got studied more and more, people began to realize that having an elevated troponin, was not specific for a myocardial infarction.  In actuality, Troponin can become elevated from a lot of other disease states that are associated with bad outcomes, such as sepsis, intracranial hemorrhage, pulmonary embolism, myocarditis, and renal failure. There are also some things that can cause elevated Troponin without worse outcomes, such as, supraventricular tachycardia, and distance/marathon runners. Troponin, therefore is not specific for myocardial infarction, but instead implies some myocardial dysfunction and/or stress.

BOTTOM LINE:  We now understand that we have to apply some clinical correlation to the meaning of elevated Troponins.

A Historical Perspective on ST-Segment Elevation in Lead aVR

When we first started talking about ST-Segment elevation in lead aVR (STE in aVR) 10 or 12 years ago, many thought it was very predictive of a Left Main Coronary Artery (LMCA) blockage with a 70% chance of getting cardiogenic shock and death. This was translated to we should consider activating the cath lab in patients with chest pain and STE in aVR.  But slowly, more literature started coming out on STE in aVR, showing that triple vessel disease and proximal LAD blockage could also cause this ECG finding, which are both very serious etiologies.  More recently it has been shown that STE in aVR is not specific for  LMCA blockage, triple vessel disease, or proximal LAD blockage, but there are some other diagnoses that could cause this finding as well.

There was a study by Kosuge et al published in American Journal Cardiology in 2005 [1], that found widespread ST-Segment depression (STD) of 1.0mm or greater to be present in 82% of individuals with 75% or greater LMCA stenosis, and only 49% of patients without LMCA stenosis. They also stated that STE 0.5mm or greater in lead aVR to be present in 78% of patients with and 14% of patients without LMCA stenosis. So this just emphasizes the fact that STE in lead aVR is not specific for LMCA stenosis.

BOTTOM LINE: Much like Troponin testing we have to apply some clinical correlation to the meaning of STE in aVR.

Some Important Points made by Amal:

  • STE in aVR Should be Concerning IF you have a patient with:
    • Worrisome/Concerning Symptoms (Cardiopulmonary Symptoms) AND…
    • ST-Segment Depression in Several Other Leads
  • Don’t worry so much about STE 0.5mm or less in lead aVR, because it lacks specificity.  Using 1.0mm or greater in lead aVR, has better specificity
  • Patients with ACS due to LMCA Blockage, Triple Vessel Disease, or Proximal LAD Blockage will look “sick” due to global cardiac ischemia.  This narrows the number of patients we would consider activating the cath lab for with STE in aVR.

What Else can Cause STE in aVR that Won’t Benefit from Going to the Cath Lab?

Worrisome Diagnoses:

  • Thoracic Aortic Dissection
  • Massive Pulmonary Embolism
  • Massive Gastro Intestinal Hemorrhage

Non-Worrisome Diagnoses:

  • Left Bundle Branch Block (LBBB)
  • Left Ventricular Hypertrophy (LVH) with Strain Pattern
  • Severe Atrial Tachydysrhythmias

LMCA Occlusion or LMCA Insufficiency?

Some physicians believe using the phrase “LMCA Occlusion” is inaccurate, because if these patients had true 100% occlusion of their LMCA, they would be in cardiogenic shock. Instead it is believed that most of these patients have at least some flow in their LMCA and the better phrase would be “LMCA Insufficiency.” Does it really matter?

Some people may assume that the term occlusion, automatically means a 100% lesion, but many use the term as 50% occlusion, 70% occlusion, etc….maybe insufficiency is a better term, but it is just a matter of semantics in the end.

What do you say to Cardiology Fellows/Attendings When they say Something to the Effect of “I don’t care About Lead aVR?”

A lot of how you approach this conversation is dependent on the relationship you already have with the cardiologist. First, explain that the patient is looking “sick” and then describe the ECG with diffuse ST Depressions and ST Elevation in aVR that concerns you for a LMCA lesion, or triple vessel disease. Some cardiologists will say OK, lets take the patient to the cath lab and others may say, this patient does not meet cath lab criteria, treat their ischemia medically and if that doesn’t work then call back. If the patient truly does have an acute LMCA lesion or acute triple vessel disease, they will not become pain free from medical therapy alone and inevitably you will end up calling the cardiologist back and telling them the patient is on maximum medical therapy, still having clinical ischemia, as well as ischemia on the ECG.

IMPORTANT POINT: Non-ST-Segment Elevation Myocardial Infarction (NSTEMI) still qualifies for emergent cath lab activation if your patient has intractable ischemia or pain, despite maximal medical therapy.

Clinical Bottom Lines:

  1. ST-Segment Elevation in Lead aVR is NOT SPECIFIC for an acute LMCA Lesion, Acute Proximal LAD Lesion, or Acute Triple Vessel Disease
  2. Correlate Your ECG with the Patient’s Clinical Status
  3. We Should use STE in aVR of ≥1.0mm as STE in aVR of ≤0.5mm is Non-Specific

References:

  1. Kosuge M et al. Predictors of Left Main or Three-Vessel Disease in Patients Who Have Acute Coronary Syndromes with Non-ST-Segment Elevation. Am J Cardiol 2005; 95: 1366 – 9. PMID: 15904646
  2. Barrabes JA et al. Prognostic Value of Lead aVR in Patients With a First Non-ST Segment Elevation Acute Myocardial Infarction. Circ 2003; 108: 814 – 819. PMID: 12885742

Post Peer Reviewed By: Matt Astin (Twitter: @mastinmd)

Chest Pain Controversies: Coronary CTA Use (Part 2)

Authors: Brit Long, MD (@long_brit, EM Attending Physician at SAUSHEC, USAF) and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW Medical Center / Parkland Memorial Hospital) // Edited by: Jamie Santistevan, MD (@Jamie_Rae_EMdoc, Admin and Quality Fellow at UW, Madison, WI)

A 53-year-old female presents with 5 hours of chest pain and diffuse weakness. She denies dyspnea, nausea/vomiting, and diaphoresis. Her vital signs, ECG, chest X-ray, and initial labs are completely normal, including troponin and TSH. You have low suspicion of PE, dissection, and other life-threatening diseases. Your center excels with coronary computed tomography angiogram (CCTA). Should you use this modality?

This is the second of a two-part series evaluating chest pain controversies in the ED. The American Heart Association (AHA) supports noninvasive cardiac imaging for further evaluation before or within 72 hours of discharge, which may consist of stress testing, CCTA, or no further testing at all.1 As discussed previously, a nonischemic ECG with negative cardiac biomarkers at 0 hr and 3 hr is associated with low risk of major cardiac adverse event (MACE).2,3 This post will examine the use of CCTA in the ED. Are there benefits? What are the adverse effects? 

Coronary computed tomography angiogram (CCTA)

CCTA has risen to the forefront of chest pain evaluation, providing an anatomical evaluation of coronary artery vasculature. This means that the test is asking one question: is there disease within the coronary arteries? It is important to note that unlike coronary angiogram, CCTA is unable to evaluate coronary blood flow.4-7 However, this test does have the potential to provide a safe, noninvasive measure that allows for a better means to diagnose CAD when compared to history, physical exam, ECG, and biomarkers.4-7

Current Guidelines

The American College of Cardiology Foundation (ACCF)/American Heart Association (AHA) and the European Society of Cardiology (ESC) guidelines list CCTA for use in patients with low or intermediate risk.4,5

Guideline Use of CCTA
ACCF/AHA – Low to intermediate risk patients, exercise capable: Class III, level of evidence C for patients with interpretable ECG. For patients with uninterpretable ECG, Class IIb, level of evidence B for CCTA.

Low to intermediate risk patients, exercise incapable: Class IIa, level of evidence C for CCTA.

– In patients with symptoms at high risk for disease, CCTA assumes a Class IIb, level of evidence C recommendation. Coronary angiogram possesses a Class I, level of evidence C recommendation.

*High risk categorized as presence of classic cardiovascular risk factors: advanced age, hypertension, diabetes mellitus, smoking, male.

ESC – Class IIa, level of evidence C recommendation for CCTA use in patients with lower range of intermediate risk as alternative to stress imaging or non-conclusive exercise ECG or stress imaging.

*Prerequisite of obtaining good imaging quality.

No role for CCTA in symptomatic patients with high pretest probability of disease.

Table 1: Current guidelines for the use of CCTA

The evidence surrounding CCTA 

The evidence for CCTA has shown a low rate of ACS/AMI within 30 days of testing, as well as decreased ED length of stay (LOS).4-10

In 2001, de Filippi et al. randomized 248 patients with normal ECG, negative biomarkers, and ages 20-65 years old to CCTA or exercise testing.8 Positive CCTA was defined by stenosis greater than 50%. Patients with negative CCTA had fewer returns (decreased by 20%) and hospital admissions (3% versus 16%) than patients with negative stress tests. The study revealed no death or MI in both groups at one year.8

The 2012 ACRIN-PA trial randomized 1,370 patients with TIMI score 0-2, ECG without ischemia, and negative first biomarker to CCTA versus standard stress test.9,11 Approximately 50% of patients in CCTA could be discharged, versus 22.7% in the stress arm, decreasing ED LOS.9

The ROMICAT-II trial evaluated CCTA and found that no coronary disease on imaging effectively ruled out ACS. However, if the CT revealed stenosis >/= 50%, sensitivity was reduced to 78.4% for ACS.12 In this population,  length of stay was 7.6 hours in the CCTA group, with a rate of ED discharge 47% in the CCTA group versus 12% in the standard evaluation arm. No difference in the rate of adverse cardiovascular events between groups was found.12

Chang et al. evaluated 32 patients who underwent repeat CCTA imaging at two years after their first imaging evaluation. No patient with less than the 50% stenosis threshold demonstrated > 50% stenosis on second imaging.13

Four large trials randomized low-risk patients to standard workup with stress testing or CCTA following ED evaluation with negative ECG and troponin.9,14-16 These studies in addition to a meta-analysis by Hulten et al. suggest decreased ED LOS, with negative predictive values approaching 99% with CCTA.17 However, no difference in MACE is found based on these large studies.9,14-17

CCTA provides sensitivities ranging from 81% to 99%, specificity 64% to 93%, positive predictive value (PPV) 64% to 92%, and negative predictive value (NPV) 83% to 99%.17-21 Obtaining these results requires an experienced reader and optimal imaging quality. A study in Canada found high variability in diagnostic capability and accuracy across four centers, questioning reproducibility when not interpreted by an experienced radiologist.21 Results demonstrate sensitivity 50% to 93%, specificity 92% to 100%, PPV 85% to 100%, and NPV 43% to 95%.21 Fractional flow reserve assessment with CCTA is a newer modality, with sensitivity 84% to 94% and NPV 72% to 80%.20-23

PROMISE

Two recent large studies have evaluated the use of CCTA in patients with chest pain. The PROMISE study randomized 10,003 patients to standard noninvasive testing or CCTA.24 This study recruited patients from outpatient settings, rather than ED, with new onset chest pain and negative biomarkers and ECG changes. No difference in death, MI, major procedural complications, or hospitalization for unstable angina between the CCTA and standard groups (3.3% versus 3.0%) was found. Patients in the CCTA group underwent more testing and intervention, 12.2% versus 8.1% for catheterization. An overall low mortality rate, 1.5%, and low rate of MI, 0.7%, were found in the population studied.24

SCOT-HEART

The SCOT-HEART trial enrolled 4,146 patients in Scotland, comparing exercise stress test versus evaluation with CCTA.25 Over 85% of patients underwent stress testing. After initial patient assessment, the physician estimated baseline risk of CAD and recommended further testing. Patients were then randomized to CCTA or standard testing only. After 6 weeks, physicians again estimated risk of CAD based on study results. In this trial, CCTA improved physician confidence in diagnosis of CAD and angina, and more patients were diagnosed with CAD in the CCTA group (23% versus 11%). This lead to more cardiac catheterizations. However, the rate of adverse cardiovascular outcomes during the follow up period of 1.7 years was not statistically different, 1.3% versus 2.0%. Patient outcomes were not affected, though physicians felt more comfortable.25

CCTA has repeatedly demonstrated the ability to decrease ED LOS. The majority of these studies incorporate low risk patients, who, with negative ECG and biomarkers, have a risk of less than 1%.2,3,26 CCTA is associated with increased rate of invasive angiography and downstream testing. The meta-analysis by Hulten et al. revealed more downstream testing, including invasive angiography.17

Muhlestein et al. evaluated close to 900 patients with diabetes type I and II, using CCTA for screening of CAD.27 Patients in the CCTA group underwent more catheterizations (13.3% versus 5.1%), more percutaneous interventions (6.0% versus 1.8%), and more bypass operations (2.9% versus 1.3%), with no change in adverse cardiac events.27 Given the increased rate of invasive testing without decreasing adverse events, use of CCTA in low risk patients is questionable.26

What is identified on CCTA?

CCTA detects coronary artery calcium and the degree of obstruction to the artery lumen. Non-obstructive CAD is that which causes <50% arterial stenosis, whereas stenosis of 50% or more defines significant CAD. Calcium plaques can be further characterized based on visual appearance and are considered at high risk for causing thrombosis if any of the following features are present: spotty calcium, remodeling of vasculature, low Housfield Units attenuation, large plaque volume and the napkin-ring sign.12 These radiographic features are based on histologic features of plaques that demonstrate high risk for rupture such as the presence of a necrotic, lipid-rich core, a thin-cap fiberatheroma and vascular remodeling.

napkin-ring

Figure 1: Cross-sectional CT showing coronary plaque with napkin-ring sign.37 a). Non-enhanced image b). Contrast-enhanced image c). Histopathology showing thin-cap fiberoatheroma with a necrotic core*.

Patient selection for CCTA

Patient selection to undergo CCTA is key for optimal imaging. Morbidly obese patients present challenges due to chest wall thickness, which interferes with imaging quality. Patients with known disease, heavy coronary calcifications, and prior coronary revascularization do not benefit. Studies demonstrate high risk patients should undergo angiogram rather than CCTA, which has better assessment of real-time coronary flow, presence of thrombotic material, and collateral circulation.28 Control of heart rate and rhythm is essential, as direct correlation exists with heart rate and ability to evaluate vasculature.29 Over 95% of coronary vasculature is evaluable with a heart rate less than 60 bpm. This decreases to 80% to 90% with rates of 60-65 bpm. As rates approach 70-80 bpm, 70% of the vasculature is evaluable.29 Patients with irregular rhythm, frequent premature atrial or ventricular ectopy, and uncontrolled tachycardia cannot be evaluated.29

Complications of CCTA

CCTA is associated increased radiation exposure, though this has decreased with improved technology. A 320-slice detector reduces radiation to 2-6 mSv.29-34 Despite this, cumulative radiation exposure increases with CCTA use due to increased downstream testing. Chronic kidney disease also warrants caution, as this test can lead to contrast nephropathy.35

Utility of CCTA

CCTA likely causes more harm than benefit in low risk patients, as it can lead to a greater number of false-positive results and further testing and increased radiation exposure.7,26  Utility of CCTA  exists for patients who may have difficulty obtaining further testing or lack of follow-up.4-8 A patient with no disease found on CCTA possesses an extremely low risk of ACS (less than 1%) and these patients can be safely discharged. No disease is found in one third to one half of low to intermediate risk patients.17 If follow-up is in place, CCTA benefit is controversial.7,17,26

If CAD of >50% stenosis is present or if there are high risk plaque features at any degree of stenosis, the patient may require aggressive medical management and should be admitted for further testing with stress test or angiography. In these cases, decision-making with a cardiologist about recommended medical or invasive management is recommended. If any degree of CAD is detected, these patients may also benefit from cardiology consult as further management should include shared decision-making with consideration of the risks and benefits of therapies and patient preferences.

Patients with intermediate risk based on history and other comorbidities may be candidates for further risk stratification with CCTA, as no disease on imaging lowers the risk of MACE.36 Further studies on the utility of CCTA for intermediate risk patients is required. Use in high risk patients should be avoided, as coronary artery disease is likely to be present on CCTA.7,26,36

Summary

– Missed ACS is a concern for patients and emergency providers. Nonischemic ECG and negative biomarker at 0 and 3 hours reduces risk of MACE to less than 1%.

– Stress testing and CCTA are commonly used for further evaluation of these patients, but their ability to further risk stratify low risk patients further is controversial.

– Use of CCTA has increased, with the goal to evaluate anatomical coronary artery disease.

– CCTA is associated with decreased ED LOS. However, CCTA is also associated with further downstream testing, with no evidence of improved outcome in low risk patients.

Intermediate risk patients, or those with difficulty obtaining follow up, may benefit from CCTA, though further studies are required in this patient subset.

References/Further Reading

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  2. Pope JH, Aufderheide TP, Ruthazer R, Woolard RH, Feldman JA, Beshansky JR, et al. Missed diagnoses of acute cardiac ischemia in the emergency department. N Engl J Med 2000; 342:1163–70.
  3. Weinstock MB, Weingart S, Orth F, VanFossen D, Kaide C, Anderson J, Newman DH. Risk for Clinically Relevant Adverse Cardiac Events in Patients With Chest Pain at Hospital Admission. JAMA Intern Med 2015 Jul;175(7):1207-12.
  4. Montalescot G, Sechtem U, Achenbach S, Andreotti F, Arden C, Budaj A, et al. 2013 ESC guidelines on the management of stable coronary artery disease: the Task Force on the management of stable coronary artery disease of the European Society of Cardiology. Eur Heart J 2013;34:2949–3003.
  5. Fihn SD, Gardin JM, Abrams J, Berra K, Blankenship JC, Dallas AP, et al; American College of Cardiology Foundation/American Heart Association Task Force. 2012 ACCF/AHA/ACP/AATS/PCnA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation 2012;126:e354–e471.
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