Tag Archives: cardiovascular

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?


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.


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.

Approach to Tachypnea in the ED Setting

Author: Dorian Alexander, MD (Associate Program Director, Director of Critical Care in Emergency Medicine, Brookdale University Hospital, Brooklyn, NY) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

Case 1:

A 19 year old female with a past medical history of asthma controlled with an albuterol inhaler presents to the ED with a chief complaint of shortness of breath. Her vital signs at triage include T 98.7F, BP 135/78, HR 108, RR 36, SpO2 100% RA.

She reports visiting a friend’s house with multiple cats and has not used her inhaler for the past two days. Today, she notes that she’s wheezing significantly, and it’s hard to breathe. Her initial peak flow is 150 with a known baseline of 350.

On exam, she’s well-appearing but tachypneic with diffuse wheezing on auscultation bilaterally without rales or rhonchi, 5 -7 word dyspnea, (+)s1s2  tachycardic without JVD, no LE edema, and an abdomen that’s soft and NT/ND.

The patient is placed on a series of nebulization treatments with albuterol and ipratropium, with improvement in her symptoms. Prednisone 60mg orally is administered, and the patient is observed for a period of time. After 3 rounds of nebulization, the peak flow has improved to 350, and she’s able to ambulate without distress in the ED. Repeat exam shows resolution of wheezing with clear lung fields bilaterally.  She’s able to be discharged from the ED with a prescription for steroids and an inhaler.


The presentation of shortness of breath is one of the most common chief complaints in the Emergency Department and primary care settings.1 Tachypnea is a symptom of an underlying process and is not a disease itself. Tachypnea in the ED is different from the subjective sensation of “shortness of breath.” Patients can be short of breath but not tachypneic.

It can be helpful to define a few terms to better understand tachypnea. Abnormally fast breathing can present as rapid shallow breathing (tachypnea) or rapid deep breathing (hyperpnea), while dyspnea refers to the sensation of shortness of breath.

A consensus statement from the American Thoracic Society defines dyspnea in the following way: “Dyspnea is a term used to characterize a subjective experience of breathing discomfort that is comprised of qualitatively distinct sensations that vary in intensity.”1

For the purpose of this discussion we will evaluate tachypnea as both rapid and deep breathing abnormalities noted on clinical presentation as a subset of a patient’s presenting symptoms inclusive of dyspnea.

The definition and clinical presentation of abnormally fast breathing should generate the following question in every clinician’s mind – why is the breathing abnormal? The answer lies in the pathophysiology of dyspnea.

Pathophysiology of Dyspnea


Fig 12

The pathophysiology of dyspnea is related to multiple complex interactions between organ systems – the respiratory, cardiovascular, neurological systems, and oxygen carriers all play a role in the development of tachypnea and dyspnea.3 Stimulation of such receptors can be achieved by direct and indirect methods leading to multiple factors simultaneously playing a role in a patient’s clinical pathology.4

Physiologic receptors of tachypnea


Fig 25

The end point of receptor stimulation is dyspnea and tachypnea.6 Primary pulmonary receptors such as wall stretch and lower airway receptors are commonly stimulated by intra-pulmonary pathologies such as COPD/Asthma/CHF; however, chemoreceptors such as medullary and carotid body receptors are often affected by extra-pulmonary factors.3,6 The identification of extra-pulmonary factors as etiologies of dyspnea is a vital aspect of the Emergency Physician’s evaluation of acute dyspnea.

Given such complex etiologies of dyspnea and tachypnea, a systematic approach to the diagnosis and management of tachypnea will more often yield an accurate diagnosis with appropriate bedside interventions.

Pulmonary Etiologies of Tachypnea

The pulmonary system is the first organ system that is evaluated at the bedside in patients with acute dyspnea and tachypnea. Primary pulmonary pathologies can be readily identified through the use of appropriate lung physical exam techniques and radiologic imaging. History, physical exam, EKG, chest x-ray, and labs as necessary can usually yield the diagnosis in the majority of cases.

The use of point of care ultrasound (POCUS) as an adjunct to bedside evaluation of pulmonary pathology in patients with dyspnea and tachypnea should be incorporated into daily practice.



Fig 3: Asthma on chest x-ray with A-Lines on lung ultrasound 7,8


Fig 4: Pneumonia on chest x-ray with lung ultrasound findings 9,10


Fig 5: Pulmonary edema on chest x-ray with diffuse B-lines on lung ultrasound 8,11


Fig 6: Pneumothorax on chest x-ray with stratosphere sign on lung ultrasound 8,12

Case 2:

A 68 year old male with a past medical history of ESRD on hemodialysis presents to the ED with acute tachypnea. His last hemodialysis session was two days ago, and the patient completed 4 hours. Vital signs at triage include T 97.6F, BP 95/55, HR 104, RR 34, SpO2 92% RA, 98% 5L NC.

On exam, the patient appears uncomfortable with mild bibasilar crackles and is tachypneic, only able to speak in intermittent sentences, (+) s1s2 muffled, (+) JVD, (+) 1 b/l LE edema. His abdomen is soft and nontender.

Bedside lung ultrasound reveals minimal B-lines with scattered A-lines and no ultrasonographic evidence of pneumothorax. Cardiac echo reveals a pericardial effusion with bowing of the right ventricle.

The patient is placed on a cardiac monitor with 5L of supplemental oxygen via nasal cannula, and his oxygen saturation increases to 98%. Intravenous fluid with normal saline is started at 100ml/hr after an initial bolus of 500ml, and his repeat BP is 128/68. Bedside EKG shows sinus tachycardia with electrical alternans. Follow up chest x-ray shows an enlarged cardiac silhouette that is increased compared to an x-ray from one month prior.

A diagnosis of pericardial tamponade is made at the bedside, and with Cardiothoracic Surgery consultation, the patient is taken to the OR for a pericardial window.

Cardiovascular Etiologies of Tachypnea

Extra-pulmonary causes of tachypnea usually pose the biggest challenge to clinicians at the bedside. The cardiovascular system should always be considered as a potential etiology of undifferentiated tachypnea. Evaluation of heart sounds with murmurs on physical exam, presence or absence of JVD, pitting edema, and hepatomegaly can all indicate a cardiac etiology of symptoms.

Screening tools such as EKG and chest x-ray may reveal findings that lead to increased suspicion for primary cardiovascular origins of a patient’s dyspnea; however, they more often yield nonspecific information.  POCUS showing pericardial effusion, tamponade physiology, diffuse B-lines, or RV > LV size may provide a higher diagnostic yield when combined with history, physical exam, EKG, and chest x-ray.13–16



Fig 7 Pericardial effusion with tamponade physiology  and electrical alternans on EKG17,18


Fig 8    RV dilation and dysfunction in acute pulmonary embolus19

Hematologic Etiologies of Tachypnea

Case 3:

A 93 year old female with a past medical history of dementia is sent to the ED for increased SOB over the past two days. At baseline, the patient is non-ambulatory, non-verbal, fed via a PEG tube, and she is a full code as per her MOLST form. Her vital signs at triage are T 96.3F, BP 90/58, HR 110, RR 32, SpO2 98% RA.

On exam, the patient is a pale-appearing elderly female with notable tachypnea, clear lungs, mildly decreased breath sounds at the bases, (+) s1s2 tachycardic with a systolic ejection murmur, a soft abdomen that’s NT/ND, normal bowel sounds, a c/d/I PEG site, rectal exam (+) melena, (+) conjunctival pallor, and loss of visualization of her palmar crease.

The patient is placed on cardiac monitoring with large bore IVs and given an initial bolus of normal saline. Her repeat BP increases to 110/68, with a reduction in her HR to 84. Her EKG and CXR show NSR and bibasilar atelectasis, respectively. Her lab work is notable for a Hgb of 4 (baseline of 8 from 1 month prior) and an INR of 2.8 (the patient is on anticoagulation for DVT). The patient is transfused two units of PRBCs in the ED, started on a PPI drip, and her coagulopathy is reversed with FFP and vitamin K. The patient is adequately resuscitated with appropriate response to transfusion and admitted to the medical intensive care unit.

Hemoglobin (Hgb) acts as the major transporter of oxygen in the blood, and an acute or chronic drop in blood Hgb concentration can reduce its oxygen carrying capacity.20 In a compensatory mechanism to maintain oxygenation, neurological and carotid chemoreceptors are stimulated to maintain oxygenation by increasing minute ventilation.20 This increase in minute ventilation appears as an acute change in a patient’s baseline respiratory effort. Anemia is an often unrecognized etiology of dyspnea and tachypnea, as pending labs can delay diagnosis. However, appropriate physical exam findings can lead to earlier recognition and intervention.21

Metabolic Etiologies of Tachypnea

Case 4:

A 9 year old male with no prior medical history presents to the ED with his mother complaining of abdominal pain.  As per his mother, he has been asking for a lot of water lately and going to the bathroom very often over the past 3 days. He developed one episode of vomiting today which progressed to abdominal pain. His vital signs at triage in include T 99F, BP 98/57, HR 120, RR 34, SpO2 100% RA, BGM – HIGH.

On exam, the patient is noted to be dehydrated and tired-appearing with deep, fast respirations and a questionable fruity odor on his breath, lungs clear bilaterally, (+) s1s2 tachycardic with no murmurs noted, a soft abdomen that is NT/ND, dry MM, and poor skin turgor.

The patient is immediately placed on a cardiac monitor with bilateral large bore IVs. A 20mg/kg fluid bolus is administered twice with labs drawn to evaluate for DKA including serum ketones and a venous blood gas. Initial results show a pH of 7.2, with a pCO2 of 16, and an anion gap of 22. The patient is immediately started on an insulin drip and admitted to the pediatric ICU for new onset diabetes and DKA.

Metabolic acidosis from a range of causes can lead to tachypnea. As the body attempts to compensate for worsening acidosis, the respiratory rate increases to reduce the pCO2 and maintain a compensated physiological pH.22 In many patients, this compensatory respiratory drive can be both visually impressive, as  patients are generating large tidal volumes and may tire due to increased work of the respiratory muscles. The compensatory respiratory rate in metabolic acidosis is the driving force behind the tachypnea and dyspnea experienced by this subset of patients. The important clinical point to always consider is correction of the underlying etiology and not the tachypnea itself. Physiologic respiratory compensation mechanisms are very efficient in maintaining a respiratory alkalosis to compensate for a metabolic acidosis; however, a patient can tire out if the underlying cause is not treated and thus rapidly decompensate with hypercarbic respiratory failure and worsening metabolic acidosis leading to life-threatening acidemia, cardiac arrest, and death. Although the causes of metabolic acidosis are multifactorial, new onset DKA is a common ED presentation that every clinician should immediately identify based on available history, physical exam, and an easily obtainable POC blood glucose.

Management & Treatment

The multifactorial nature of tachypnea and dyspnea leads to complex management and treatment options depending on the underlying process involved. The primary goal is to always treat the primary etiology and support the respiratory system via adjunctive therapies as necessary. The detailed management of all causes of tachypnea is beyond the scope of this discussion; however, we can make some broad generalizations by organ system.

Pulmonary: Adjunctive respiratory support in the form of inhaled beta agonists and anticholinergics for bronchospasm induced disease states with additional steroids to reduce inflammation over time are the mainstay in asthma and COPD exacerbations. Diuretics work to reduce extravascular fluid in CHF states, and nitrates can assist in fluid redistribution for CHF. It’s important to note that these medications often do not provide instant relief, and patients in acute distress from bronchospastic disease or acute pulmonary edema might benefit from the initiation of non-invasive ventilation in the form of BIPAP or CPAP. Laboratory studies, although not always necessary in reversible exacerbations of asthma, might include CBC, BMP, a blood gas, troponin, and BNP. Radiologic studies in the form of chest x-ray combined with bedside lung ultrasound often confirm the diagnosis.

Cardiovascular: Cardiac causes may overlap with pulmonary etiologies: for example, an NSTEMI leading to decompensated CHF. Although workup strategies may be similar, the addition of bedside cardiac ECHO can reveal important diagnostic information. The presence of a pericardial effusion and tamponade physiology will lead to emergent changes in bedside management. RV: LV > 0.9 raises clinical suspicion for PE, and thus additional diagnostic testing such as a bilateral LE duplex and a CTA of the chest could be performed leading to earlier diagnosis and treatment.

Hematologic: Hematologic emergencies can have a broad range of management options and treatment modalities, not all of which are available in the ED. Symptomatic anemia however, is one medical emergency that should be recognized by the Emergency Physician and treated with appropriate blood product transfusion in the form of PRBCs, FFPs, and platelets as necessary.

Metabolic: Tachypnea and dyspnea from metabolic causes are a direct compensatory mechanism due to the underlying acidosis. A comprehensive differential for the evaluation of metabolic acidosis is beyond the scope of this discussion, but common etiologies such as DKA, which is managed with IVF resuscitation and initiation of insulin therapy to correct the anion gap acidosis must be recognized at the bedside for early initiation of therapy and reversal of acidosis. Other causes of metabolic acidosis, especially those related to renal failure or potentially lethal toxic overdoses, may require hemodialysis for correction.

Summary & Take Home Points

Tachypnea can be the presentation of multiple different pathologies. A focused history and physical exam, along with an understanding of the pathophysiology of appropriate disease states, can lead to thorough evaluation and management at the bedside. A systematic organ system approach to the patient can quickly lead to bedside diagnosis and initiation of treatment in patients with undifferentiated tachypnea.

As Emergency Physicians we should:

  • Avoid anchoring on the pulmonary system as the only cause of tachypnea
  • Maintain a broad differential for extra-pulmonary causes of tachypnea
  • Use bedside ultrasound in the setting of undifferentiated tachypnea; lung US can reveal pathology of PTX, Asthma, CHF, and PNA effectively and accurately
  • Utilize follow up chest x-ray to improve diagnostic ability
  • Combine EKG findings with bedside ECHO to quickly identify life threatening conditions
  • Remember that metabolic acidosis can present as tachypnea & point of care testing can give clues to an early diagnosis of DKA


References/Further Reading:

  1. Parshall MB, Schwartzstein RM, Adams L, et al. An official American thoracic society statement: Update on the mechanisms, assessment, and management of dyspnea. Am J Respir Crit Care Med. 2012;185(4):435-452. doi:10.1164/rccm.201111-2042ST.
  2. Laviolette L, Laveneziana P. Dyspnoea: A multidimensional and multidisciplinary approach. Eur Respir J. 2014;43(6):1750-1762. doi:10.1183/09031936.00092613.
  3. Ashton MD R, Raman MD D. Dyspnea. http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/pulmonary/dyspnea/. Published 2015. Accessed June 11, 2016.
  4. Sharma V, Fletcher SN. Review Article. N Engl J Med. 2014;333(23):1-9. doi:10.1111/anae.12709.
  5. Kabrhel C. Approach to the Patient with Undiffrentiated Dyspnea.; 2012.
  6. Burki NK, Lee LY. Mechanisms of Dyspnea. Chest. 2010;138(5):1196-1201. doi:10.1378/chest.10-0534.
  7. Bickle I. Hyperinflated lungs in Asthma. https://radiopaedia.org/cases/hyperinflated-lungs.
  8. Touw HRW, Tuinman PR, Gelissen HPMM, Lust E, Elbers PWG. Lung ultrasound: Routine practice for the next generation of internists. Neth J Med. 2015;73(3):100-107.
  9. Kwong Y. Pneumonia. https://radiopaedia.org/cases/klebsiella-pneumonia-1.
  10. Zhan C, Grundtvig N, Klug BH. Performance of Bedside Lung Ultrasound by a Pediatric Resident A Useful Diagnostic Tool in Children With Suspected Pneumonia. Pediatr Emerg Care. 2016;0(0):1-5.
  11. Dixon A. CHF. https://radiopaedia.org/cases/pulmonary-oedema-5.
  12. Jaff M. Pneumothorax. https://radiopaedia.org/cases/pneumothorax-14.
  13. Lichtenstein DA. BLUE-Protocol and FALLS-Protocol. Chest. 2015;147(6):1659-1670. doi:10.1378/chest.14-1313.
  14. Ultrasonography P, Moore CL, Copel JA. Point-of-Care Ultrasonography. N Engl J Med. 2011;364(8):749-757. doi:10.1056/NEJMra0909487.
  15. Koenig S, Chandra S, Alaverdian A, Dibello C, Mayo PH, Narasimhan M. Ultrasound assessment of pulmonary embolism in patients receiving CT pulmonary angiography. Chest. 2014;145(4):818-823. doi:10.1378/chest.13-0797.
  16. Bataille B, Riu B, Ferre F, et al. Integrated use of bedside lung ultrasound and echocardiography in acute respiratory failure: a prospective observational study in ICU. Chest. 2014;146(6):1586-1593. doi:10.1378/chest.14-0681.
  17. Maung M. Khin Hou R, I. Martin A, A. Bassily E, Coffman GJ, A. Siddique M, M. Whitaker D. Redistribution of pericardial effusion during respiration simulating the echocardiographic features of cardiac tamponade. Int J Case Reports Images. 2016;7(4):261. doi:10.5348/ijcri-201645-CR-10633.
  18. Roediger J. Electrical Alternans. http://ecgguru.com/ecg/electrical-alternans. Published 2012.
  19. Presently E, Tte E, States U. Role of Echocardiography in Patients with Acute Pulmonary Thromboembolism. Journal of Cardiovascular Ultrasound. 2008;16(1):9-16.
  20. Ferrari M, Manea L, Anton K, et al. Anemia and hemoglobin serum levels are associated with exercise capacity and quality of life in chronic obstructive pulmonary disease. BMC Pulm Med. 2015;15:58. doi:10.1186/s12890-015-0050-y.
  21. Santra G. Usefulness of examination of palmar creases for assessing severity of anemia in Indian perspective: A study from a tertiary care center. Int J Med Public Heal. 2015;5(2):169. doi:10.4103/2230-8598.153830.
  22. Ingelfinger JR, Seifter JL. Disorders of Fluids and Electrolytes Integration of Acid–Base and Electrolyte Disorders. N Engl J Med. 2014;19371(6):1821-1831. doi:10.1056/NEJMra1215672.


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:



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.



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:




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.


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.

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)


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:


(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…


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.


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


-Congenital Heart Disease

-Prior Cardiac Surgery


-Arterial Dissection (Aorta, Coronary, Carotid)

Infectious -Myocarditis

-Lyme Disease



-Typhoid Fever*

-Legionnaires disease*





-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**






-Organophosphate poisoning


-Carbamate insecticide poisoning


-Tricyclic Antidepressant Poisoning


-Levetiracetam overdose


Other -Heat exhaustion/stroke



-Increased Intracranial Pressure

-Spinal Cord Injury

-Carotid hypersensitivity syndrome

-Chromosome 19p duplication syndrome

-Fleisher syndrome

-Young Simpson syndrome

-Asphyxia neonatorum


-Lupus Carditis

-Oculocardiac Reflex



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:


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


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


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.


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.


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.


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.

BNP Level in the Emergency Department: Does it Change Management?

Authors: Michael Lamberta, MD (@EMLamberta, EM Senior Resident Physician, Jacobi / Montefiore Medical Center, Bronx, NY) and Andrew Chertoff, MD (@AChertoff, Site Director, EM Attending, Montefiore Medical Center) // Edited by: Jennifer Robertson, MD, MSEd and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)


Evaluating the acutely dyspneic patient conjures a range of differential diagnoses and treatment algorithms.  Often a simple history will suggest the etiology, such as a patient with a 50 pack- year history of smoking, on home oxygen (O2), with worsening cough and accessory muscle use. Other examples include the nursing home patient who aspirated a day ago and is now febrile, or the patient with a history of heart failure (HF) who ran out of his daily furosemide. On the other hand, patients with multiple comorbidities, overlapping signs and milder symptoms can generate diagnostic uncertainty when evaluating dyspneic patients in the Emergency Department (ED).


A 58 y/o male w/ PMH of Atrial flutter (AFL), coronary artery disease (CAD), hypertension (HTN), diabetes mellitus (DM), and morbid obesity is sent to the ED from his Primary Care Physician’s (PCP) office after reviewing the results of his recent sleep study. The patient complains of progressive shortness of breath (SOB) x 1 week. Because his PCP was concerned about his SOB, he presented to the ED for evaluation. Over the last week, the patient states that he has been sleeping sitting up, has had difficulty speaking in full sentences, and complains of dyspnea on exertion. Although he denies previous fever or worsening cough, he currently feels chilly and feverish.  He notes mild worsening of lower extremity swelling although not as severe as previous admissions. The patient denies headache (HA), dizziness and palpitations. He states he is taking his home medications as prescribed.

The patient denies illicit drug use and he has never smoked tobacco.

Medications: Atenolol, Diltiazem, isosorbide mononitrate, losartan, metformin, simvastatin, warfarin

What is BNP?

Brain or B-Type Natriuretic Peptide (BNP) is an What is BNP?

Brain or B-Type Natriuretic Peptide (BNP) is an endogenous peptide hormone secreted from ventricles that have elevated end-diastolic pressure or increased ventricular volume.   Release of this peptide into circulation cues systemic effects and mediates the neurohormonal responses of Acute Decompensated Heart Failure (ADHF).

Pearl: Nesiritide is recombinant BNP that has been studied for the treatment of ADHF.


What are the Biomarkers?

Natriuretic Peptide (NP) assays gained approval by the FDA around the year 2000 for the evaluation of undifferentiated dyspnea and suspected ADHF.  The first commercially available test detected the biologically active hormone BNP, but many more recent assays also detect the inert Amino-terminal cleavage product of the BNP prohormone: N-Terminal proBNP (NT-proBNP) (Table 1).  Both biomarkers are comparable in their diagnostic accuracy demonstrated by Receiver Operating Characteristic (ROC) curves. [1] Fifteen years after their commercial introduction, these biomarkers are now a routine part of ED dyspnea order sets, but have we seen this translate into a change in patient management?


  • The half-life of NT-proBNP is 4-5x longer than BNP contributing to higher diagnostic cut-offs of NT-proBNP.
  • NT-proBNP proceeds through renal clearance, whereas BNP is neutralized. Although both are elevated in renal failure NT-proBNP is more sensitive to decrease in GFR.
  • Nesiritide will be detected through BNP assay, but will not confound NT-proBNP testing,


Case cont:

Physical Exam

Vital signs: Temperature (T)98.2° Farenheit (F), Pulse (P) 106 beats per minute (bpm),         Blood pressure (BP) 150/100, respiratory rate (RR) 24, Oxygen saturation 93% on     room air (RA)

General: Obese 167 kilograms (kg), sitting up in stretcher in mild distress

Neck: Jugular venous distention (JVD) evaluation limited by body habitus

Pulmonary: Visibly SOB, Decreased breath sounds at bases. No wheezing.

Cardiovascular: tachycardic and irregular

Abdomen:    Obese, non-tender (NT)

Extremities:    Full range of motion at joints, no effusions. 2+ pitting edema up to knees.

Neurological: Alert & Oriented x3, Speech fluent

ACEP Clinical Policy  (2007)Level B recommendations.

The addition of a single BNP or NT-proBNP measurement can improve the diagnostic accuracy compared to standard clinical judgment alone in the diagnosis of acute heart failure syndrome among patients presenting to the ED with acute dyspnea. Use the following guidelines:

·         BNP <100 pg/mL or NT-proBNP <300 pg/mL acute heart failure syndrome unlikely (Approximate LR- = 0.1)

·         BNP > 500 pg/mL or NT-proBNP >1,000 pg/mL acute heart failure syndrome likely (Approximate LR+ = 6)

Do Natriuretic Peptides (NPs) Improve Diagnosis in the ED?

Since 2001, multiple trials have sought to establish the diagnostic accuracy of NPs relative – and in addition – to routine physician evaluation. While these studies do not specifically address the effects of NP testing on patient management, it has been shown that NPs add little value to an Emergency Physician (EP)’s diagnosis of heart failure.  This is best expressed in a review on heart failure that concluded, “For patients with classic signs of ADHF (i.e. prior episodes of ADHF, volume overload, dyspnea, and orthopnea) or those with shortness of breath consistent with other etiologies (i.e. asthma, COPD), BNP is not likely to assist in the diagnostic workup. Checking BNP levels in indeterminate cases may aid in diagnosing or excluding ADHF, but results may leave the EP with additional questions.”[2]  Several derivation trials and associated analyses also support this conclusion [3,4,5,6,7,8]. Still, this is not to say that NPs have no utility in patient evaluation, especially in more equivocal cases.

What are the outcomes?

As emergency physicians, we should recognize how the potential application of a test may change patient management plans and outcomes, and/or contribute to societal costs.

Most conversation about NPs extrapolates on anecdotal evidence. Without a standardized use, it is difficult to study how knowledge of NP biomarkers may influence the outcomes of a patient’s clinical course.  Accordingly, there have only been 7 large randomized controlled trials (RCTs) evaluating how clinician’s knowledge of NP results may have an effect on patient outcomes. [4,9,10,11,12,14,15]  In addition, these RCTs have largely evaluated patient disposition, length of stay, cost of care, 30-day re-admissions, and mortality.

Does BNP change disposition?

The B-type Natriuretic Peptide for Acute Shortness of Breath EvaLuation (BASEL) was one of the earliest RCTs to evaluate outcomes.  The study found a reduction in percentage of admissions 85% vs 75% in the BNP group, and similar reduction in ICU admission 24% vs 15%.  The authors did not provide data about baseline history of heart failure between groups, but found similar final diagnoses of heart failure (45% BNP group, 51% Control group).  There was, however, a significant difference in the number of patients ultimately diagnosed with chronic obstructive pulmonary disease (COPD) in the test group (23% vs 11%), which raises the issue of potential selection bias.  One would think with proper randomization, the discharge diagnoses between groups would be similar, but that knowledge of BNP may decrease time to make the diagnosis.  Yet, this significant difference in final diagnosis between groups may have contributed to the length of stay, especially if COPD patients recovered faster. [9] Another study in the Netherlands found that the ED clinician’s knowledge of NT-proBNP showed a similar trend, although not statistically significant, toward decreased admission rates in the BNP group (62% vs 67%).  However, this sample represented a younger cohort (mean age 58.2 years), and the admission rates of 62 and 67% were, overall, comparatively lower than other studies. [10] Several other studies recruited patients with mean ages of (65-74) and reported higher overall admission rates of 85-90%.  These older populations consistently showed no statistical difference in admission rates between the BNP and non-BNP groups. [4,11,12,14,15] These results likely reflect the reality that when older patients present to the ED with acute dyspnea, they are often sicker. Thus, the majority will require admission regardless of cause and the outcomes of BNP testing.

Does BNP testing decrease length of stay?

The provocative BASEL study further demonstrated a significant decrease in time to discharge for patients who received BNP testing (8 vs 11 days). [9]  A cohort in the Netherlands yielded somewhat equivocal results with a 2-day decrease (1.9 vs 3.9) in “time to discharge” from entry to the ED, but this study did not find a significant difference in the length of stay for admitted patients.  Three subsequent studies and a meta-analysis of available data could not find any significant difference in length of stay for patients evaluated by NT-proBNP. [4,11,12,13,14,16]

Does it Save Money?

It is not surprising that the 2 RCTs that found decreased time until discharge also found a decrease in the cost per patient (Rutten et al. and BASEL).  As shorter hospital stays will lower the bill, the trials that showed decreased time in hospital in the BNP group also found an average savings just above $1,000. [9,10]  Moe et al. also measured a savings of approximately $1,000 despite no difference in length of stay (LOS), but perhaps accounted for by the decreased number of readmissions (35%) over 60 days.  It should be noted, however, that the lead author received significant funding from Roche Diagnostics, which is the biomarker manufacturer. [4] Still, there were no significant cost differences reflected in un-biased RCTs evaluating populations in heterogeneous healthcare systems. [11,12,15]

Does it Change Therapy?

Anecdotally, BNP has been promoted for its strength to discriminate between COPD, pneumonia, and heart failure, but so far, no studies have clearly demonstrated that it has helped reduce the use of “inappropriate therapy”. Schneider et al. was the only trial to comment “Knowledge of BNP levels did not change the use of bronchodilators, diuretics, vasodilators, antibiotics, steroids, angiotensin-converting enzyme inhibitors, and noninvasive ventilation, and use of appropriate heart failure medication was not increased in patients with heart failure in the BNP group versus the control group.”[11] The authors did not provide data on this finding, but in the case of dyspneic patients in the ED, most clinicians will broadly cover the patient for multiple conditions based on more specific evaluations such as chest x-ray findings, volume status, or hypercarbia.

Does it Decrease Mortality? 

There was no difference in 30-day mortality in any of the RCTs that measured this outcome including the BASEL trials. [4,9,10,12]  The Rapid Emergency Department Heart Failure Outpatients Trial (REDHOT) took another approach by evaluating prognostic value of BNP.  The study found that patients with BNP values >200pg/mL had worse 90-day outcomes including mortality, cardiac readmissions, and cardiac ED visits concluding that severe elevation in BNP can help to better stratify those who are at risk for adverse outcomes. [14]  The REDHOT II trial attempted to bare these results out by studying the use of serial BNPs in admitted patients.  This trial did not prove to show significant improvement in mortality, readmission rate, or length of stay. Alternatively, authors found renal function and hemodynamics to be more closely associated with in-hospital 30-day mortality than serial measurements of BNP. [15]

Case Cont. Chest X-Ray

Compared to X-ray 2 years prior, there is interval development of bilateral lower lobe opacities.  The hilar and mediastinal contours are normal. Heart is mildly enlarged. There is no pneumothorax.  The lateral costophrenic angles are sharp.


The BASEL and the IMPROVE-CHF trials showed significant reduction in costs and admissions, but had questionable conflicts of interest, generalizability and/or sample imbalance. Later RCTs showed no difference in relevant outcomes. RCTs are inconclusive for the routine use of BNP in the evaluation of dyspnea in the ED.Take-Aways:

  • BNP is promoted in cases of uncertainty. Despite the potential use of BNP to reduce costs by decreasing admissions, it is uncertainty alone that often dictates whether a dyspneic patient is admitted, irrespective of heart failure or BNP level.
  • Up to 90% of patients in older study cohorts were admitted, which likely reflects that most patients with ADHF are older, sicker and likely chronically ill patients who will require admission regardless of the etiology of the dyspnea.
  • Prognosticating: Elevated BNP almost always suggests a poor prognosis whether it is used to stratify ADHF, non-ST elevation myocardial infarction (MI), or PE, but prognosis is often more accurately reflected – and more easily assessed – by patient hemodynamics and renal perfusion. [14,17,18] There is no strong evidence that BNP will consistently help an admitting team in their management, but there is still ongoing research that is attempting to discern how BNP may help in response-guided therapy and discharge planning.
  • Ruling-in: Some suggest BNP as a rule-in test to diagnose patients who are being treated erroneously for other conditions, such as a 65-year-old patient with a history of COPD. Rosen even suggests “we abandon the routine obtaining of a BNP level for patients deemed to be having a CHF flare-up, and instead consider it in all dyspnea patients that we do not believe have CHF.” [19] This method of screening for heart failure is not a common application, and has not been systematically studied, but could drastically change treatment course.
  • Ruling-out: As expenditures for heart failure continue to soar, the use of BNP, in concert with other clinical signs and adjunct studies, may have significant application for ruling-out ADHF in known HF patients. This may help identify patients who are safe for outpatient management.  Some studies have attempted to derive scoring methods for this purpose.

PIC3 BNP.jpg

  • The “gray zone”: Likely BNP will continue to find application on a   case-by-case basis by the ED clinician who is interested in detecting the presence of heart strain or not. Interpretation of BNP should be considered after establishing pre-test probability for the patient, with the knowledge of confounding variables (Table 2). Clinicians can also employ tools to interpret the test like that proposed by Steinhart et al. (available for download here). [21]  That said, some cases of intermediate probability may represent the complex and sicker patients who requiring longer hospital stays and extended work-ups. In these cases, more than half the time, the knowledge of BNP will unlikely help narrow the diagnosis. [21]
  • Although anecdote may support BNP in certain cases, based on the current trials, there is little evidence to show that this biomarker has the potential to change management that will lead to clinically significant outcomes.
Case Cont. Lab Data

Venous Blood Gas

pH 7.292  pCO2 74 pO2 31 HCO3 35

Lactate          1.0 mmol/L

Troponin         Negative

NT-proBNP     718 pg/mL

Case Conclusion:  This 58yo man has some unfortunate chronic conditions that could be contributing to his dyspnea.  Based on history, a mild CHF was suspected.  However, he was visibly short of breath and the venous blood gas (VBG) revealed a carbon dioxide (CO2) level of 74 mm Hg and therefore, non-invasive positive pressure ventilation (NIPPV) and steroids were initiated.  Despite no history of fever, productive cough or elevated white count, the chest X-ray demonstrated bi-basilar infiltrates and antibiotics were provided.   The patient had trace edema, hypertension and worsening orthopnea, so the clinicians also administered IV furosemide. The patient was promptly admitted.

The patient’s NT-proBNP of 718 pg/mL proved lower than his previous episode of ADHF two years prior (1354 pg/mL), but higher than a level obtained during routine follow-up one year prior (178 pg/mL).  This patient is diagnostically complex and identifies the prototypical “gray zone” patient who may have one, but more likely three, pathologies inciting dyspnea.  Not to mention, the patient’s obesity may falsely lower BNP, whereas Cor Pulmonale from obstructive sleep apnea (OSA) or pulmonary hypertension may elevate BNP independent of left ventricular (LV) volume overload.  Plus, in cases of precipitous pulmonary edema, BNP may not be appreciably elevated at all.  This patient was admitted and despite elevated blood pressure in the ED, he became septic during hospitalization from the pneumonia. One could say that the absence of a largely elevated BNP made it easier to cover for antibiotics in a patient without fever or white count but only a suggestive x-ray, while others would say it just reflected the initial uncertainty of the clinician.  Independent of BNP level, the clinical presentation and adjunct studies dictated the decision to initiate broad-coverage therapy for CO2 retention (NIPPV, steroids), volume overload (NIPPV, Lasix), and pneumonia (Antibiotics).

References / Further Reading

  1. Mueller TT. Head-to-head comparison of the diagnostic utility of BNP and NT-proBNP in symptomatic and asymptomatic structural heart disease. Clinica chimica acta. 2004-03;341:41-48.
  2. JM Kosowsky, JL Chan. Acutely Decompensated Heart Failure: Diagnostic and Therapeutic Strategies. EB Medicine Review (2006). https://www.ebmedicine.net/topics.php?paction=showTopic&topic_id=87
  3. McCullough PA, Nowak RM, McCord J, et al. B-type natriuretic peptide and clinical judgment in emergency diagnosis of heart failure: analysis from Breathing Not Properly (BNP) Multinational Study. Circulation 2002;106:416–22.
  4. Moe GW, Howlett J, Januzzi JL, Zowall H, for the Canadian Multicenter Improved Management of Patients With Congestive Heart Failure (IMPROVE-CHF) Study Investigators. N-terminal pro-B-type natriuretic peptide testing improves the management of patients with suspected acute heart failure: primary results of the Canadian prospective randomized multicenter IMPROVE-CHF study. Circulation 2007;115:3103–10
  5. Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med. 2002;347:161-167.
  6. Januzzi JL Jr, Camargo CA, Anwaruddin S, et al. The N-terminal Pro-BNP Investigation of Dyspnea in the Emergency Department (PRIDE) study. Am J Cardiol. 2005;95:948-954.
  7. Wang CS, FitzGerald JM, Schulzer M, Mak E, Ayas NT. Does this dyspneic patient in the emergency department have congestive heart failure? JAMA 2005;294:1944–56
  8. Schwam E. B-type natriuretic peptide for diagnosis of heart failure in emergency department patients: a critical appraisal. Acad Emerg Med. 2004;11:(6)686-91.
  9. Mueller C, Scholer A, Laule-Kilian K, et al. Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea. N Engl J Med 2004;350:647–54
  10. Rutten JH, Steyerberg EW, Boomsma F, van Saase JL, Deckers JW, Hoogsteden HC, et al. N-terminal pro-brain natriuretic peptide testing in the emergency department: beneficial effects on hospitalization, costs, and outcome. Am Heart J 2008;156(1):71-7
  11. Schneider HG, Lam L, Lokuge A, et al. B-type natriuretic peptide testing, clinical outcomes, and health services use in emergency department patients with dyspnea: a randomized trial. Ann Intern Med 2009;150:365–71.
  12. Meisel SR, Januzzi JL, Medvedowski M, et al. Pre-admission NT-proBNP improves diagnostic yield and risk stratification – the NT-proBNP for Evaluation of dyspneic patients in the Emergency Room and hospital [BNP4EVER] study. Acute Cardiovas Care 2012
  13. Trinquart L, Ray P, Riou B, Teixeira A. Natriuretic peptide testing in EDs for managing acute dyspnea: a meta-analysis. Am J Emerg Med. 2011;29:(7)757-67.
  14. Maisel A, Hollander JE, Guss D, et al. Primary results of the Rapid Emergency Department Heart Failure Outpatient Trial (REDHOT). A multicenter study of B-type natriuretic peptide levels, emergency department decision making, and outcomes in patients presenting with shortness of breath. J Am Coll Cardiol. 2004 Sep 15. 44(6):1328-33.
  15. Singer AJ, Birkhahn RH, Guss D, et al. Rapid Emergency Department Heart Failure Outpatients Trial (REDHOT II): a randomized controlled trial of the effect of serial B-type natriuretic peptide testing on patient management. Circ Heart Fail 2009;2:287–93
  16. Lam LL, Cameron PA, Schneider HG, et al. Meta-analysis: effect of B-type natriuretic peptide testing on clinical outcomes in patients with acute dyspnea in the emergency setting. Ann Intern Med 2010; 153: 728−735.
  17. Heeschen C, Hamm CW, Mitrovic V, et al. N-terminal pro-B-type natriuretic peptide levels for dynamic risk stratification of patients with acute coronary syndromes. Circulation. 2004 Nov 16. 110(20):3206-12.
  18. Binder L, Pieske B, Olschewski M, et al. N-terminal pro-brain natriuretic peptide or troponin testing followed by echocardiography for risk stratification of acute pulmonary embolism. Circulation. 2005 Sep 13.
  19. Carpenter CR, Keim SM, Worster A, Rosen P, BEEM (Best Evidence in Emergency Medicine). BRAIN NATRIURETIC PEPTIDE IN THE EVALUATION OF EMERGENCY DEPARTMENT DYSPNEA: IS THERE A ROLE? The Journal of Emergency Medicine. 2012;42(2):197-205.
  20. Emergency Medicine Journal Club. Does BNP Augment Acute Decompensated CHF ED Management? WUSM-St. Louis. Journal Club November, 2009. http://emed.wustl.edu/education/EmergencyMedicineJournalClub/Archive/November2009.aspx
  21. Steinhart B, Thorpe KE, Bayoumi AM, Moe G, Januzzi JL, Mazer CD. Improving the diagnosis of acute heart failure using a validated prediction model. J Am Coll Cardiol 2009;54:1515–21.


  1. LB Daniels, AS Maisel. Natriuretic Peptides. J Am Coll Cardiol. 2007 Dec 18. 50(25): 2357-68. (Tables 1-2)

2. 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;49:627–69. (BNP Clinical Policy)  http://www.acep.org/workarea/DownloadAsset.aspx?id=8778

Management of Atrial Fibrillation: Do’s and Don’ts

Author: Courtney Cassella, MD (EM Resident Physician, Icahn School of Medicine at Mount Sinai) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

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  • AF – Atrial fibrillation
  • Paroxysmal – Terminates spontaneously or with intervention within 7d
  • Persistent – Continuous >7d
  • Long-standing persistent – >12mo
  • Permanent – Persistent for which cardioversion has failed or has not been attempted
  • Nonvalvular – AF in absence of rheumatic mitral stenosis, a mechanical or bioprosthetic heart valve, or mitral valve repair
  • BB – β-blocker
  • CCB – Nondihydropyridine Calcium Channel Blocker


When a patient presents in new onset or rapid AF, a priority should be to identify and treat underlying disease or precipitating factors. The PIRATES mnemonic is a helpful reminder although it is not complete.

=>PIRATES mnemonic

Pulmonary disease (COPD, PE)

Ischemia (ACS)

Rheumatic heart disease (mitral stenosis)

Anemia (high output failure/tachycardia)/Atrial Myxoma



Sepsis/Sick Sinus Syndrome


=>Causes not included in the mnemonic:

Electrolyte abnormalities

Congestive heart failure



High sympathetic tone states: sepsis, post-operative, hypovolemia


Acute Management

=>Rate versus Rhythm Control  

The RACE1, 2 and AFFIRM3 studies demonstrate rhythm-control has no survival benefit over rate-control. It is prudent to purse rate control in the acute setting since it is contraindicated to cardiovert stable patients with AF >48 hours or unknown duration without anticoagulation. Therefore, for stable patients without pre-excitation, intravenous BB or CCB are recommended to slow rapid AF.4-12


=>β-Blocker (BB) versus Nondihydropyridine Calcium Channel Blocker (CCB)

Between a BB and CCB, which is the best medication? The decision often encompasses multiple factors including contraindications, physician comfort, home medications, pharmacodynamics, etc.

In regards to home medications, it may benefit patients to continue the same class of home medication. Mixing BB and CCB, although sometimes necessary for rate control, may act synergistically potentiating AV nodal blockade, bradycardia, and hypotension.13-15


  • β-Adrenergic Antagonist16
    • β 1 (80% cardiac β receptors) receptor stimulation
      • Increases inotropy and chronotropy
    • β 2 receptor stimulation
      • Increases inotropy, relaxation, and chronotropy
      • Mediates bronchodilation
      • Decreases systemic vascular resistance
    • Mechanism: Blocks β -adrenergic stimulation
    • β 1 selective antagonist – decrease inotropy and chronotropy
      • Esmolol
        • Shortest half life (T1/2 8 minutes)
        • No oral formulation
        • Adverse reactions: dose dependent hypotension that resolves after 30 minutes of discontinuation5, 8
      • Metoprolol
        • T1/2 3-4 hours
        • Oral formulation both short and long acting
      • Atenolol
        • T1/2 5-9 hours
        • Oral formulation
      • Carvedilol
      • Additional: Acebutolol, Betaxolol, Bisoprolol, Celiprolol, Nebivolol
    • Contraindications:
      • Active wheeze in reactive airway disease (asthma, COPD) – Although β 1-blockers are cardioselective, studies demonstrate they decrease FEV1 and PEFR. Therefore BB should be used with caution in severe or active reactive airway disease.17, 18
      • Known II or III degree AV block – BB or CCB may cause II or III degree AV block in 15% of patients.15


  • Non-dihydropyridine Calcium Channel Blocker19
    • 4 classes of CCBs, but nondihydropyridines have the greatest affinity for myocardial calcium channels
    • Mechanism: Impedes calcium influx and channel recovery in the myocardium
      • Inhibitory effect on SA and AV nodal tissue
    • Nondihydropyridines
      • Diltiazem
      • Verapamil
        • More potent negative inotrope > more profound side effect of hypotension8
      • Contraindications:
        • Decompensated heart failure as CCBs may lead to further hemodynamic compromise4, 20, 21 (for more continue below)
        • Known II or III degree AV block – BB or CCB may cause II or III degree AV block in 15% of patients.15

Metoprolol and diltiazem are the most commonly used BB and CCBs given their oral formulation and relative hemodynamic stability. There are two prospective studies directly comparing metoprolol and diltiazem. Fromm et al found diltiazem may provide superior rate control compared to metoprolol with no adverse events noted (no episodes of hypotension or bradycardia).12 It is important to note the inclusion/exclusion criteria of the studies.

  • Inclusion: ventricular rate ≥120 bpm, SBP ≥90 mmHg
  • Exclusion: SBP <90mmHg, ventricular rate ≥220 bpm, QRS >0.100s, 2nd or 3rd AV block, STEMI, NYHA Class IV HF, active wheezing with history of asthma/COPD, anemia (hemoglobin <11 g/dL), pregnancy.

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DO consider amiodarone in critically ill patients. DON’T use amiodarone in AF >48 h or unknown duration without anticoagulation.

In cases where BB or CCB fail to reduce the heart rate or induce hypotension, amiodarone may be a reasonable option. Although amiodarone is an anti-arrhythmic, it has AV nodal blocking properties. An AHA class IIa recommendation states amiodarone can be used for rate control in critically ill patients.4 (Three studies provide the basis for this recommendation6, 22, 23)

  • Class III antiarrhythmic
    • Use in chemical cardioversion
  • Sodium and potassium channel blocking properties
  • β -blocking and calcium channel blocking properties => slows conduction through the AV node.
  • Considerations: Amiodarone is an anti-arrhythmic, therefore in cases of AF or flutter >48h of unknown duration there is a possibility of cardioversion and risk of stroke.
  • Pulmonary, hepatic, and thyroid toxicity

Clemo et al studied amiodarone for acute rate control in 33 ICU patients with hemodynamically destabilizing atrial tachycardia. This retrospective chart review targeted a cohort who failed conventional therapy including BB, CCB, digoxin, electrical cardioversion, and procainamide pharmacologic cardioversion. Amiodarone therapy was associated with a decrease in rate and increase in systolic blood pressure. Furthermore, there were no reported events of hypotension or bradycardia, possibly secondary to a lower loading dose of 2-3mg/kg. Of note, a significant amount of patients converted to sinus rhythm while on amiodarone infusion (29 at 24 hours, 20 at discharge).22


Table of Common Rate Control Agents via AHA/ACC/HRS Guidelines4

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=>Goals of Rate Control: DO aim for ventricular rate less than 110 bpm.

Earlier guidelines recommend the goal heart rate to be less than 80 bpm. RACE II provided the basis for a lenient rate-control strategy by investigating a resting heart rate <110 bpm versus <80 bpm. RACE II found lenient-control was non-inferior to strict-control for composite death from cardiovascular causes, hospitalization for heart failure, stroke, systemic embolism, major bleeding, arrhythmic events (syncope, sustained VT, cardiac arrest, life-threatening adverse effects of drugs, implantation of pacemaker or ICD). 24

  • Asymptomatic/hemodynamically stable: <110 bpm
  • Symptomatic: Rate to point of asymptomatic

=>Electrical Cardioversion (Unstable AF): DO cardiovert unstable AF.

Patients with hemodynamic instability, ongoing ischemia, or worsening heart failure should undergo direct current cardioversion.4 If the choice is available, biphasic waveform devices have greater efficacy than monophasic.25, 26 In terms of the selection of energy level, Mittal et al provides a protocol for escalating shock energies on monophasic and biphasic devices with reported efficacy of each energy level.26 Some advocate starting at maximum energy to optimize success as studies have shown higher energy does not increase cardiac injury.27, 28

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In regards to pad placement, a systematic review by Kirkland et al found no difference in anterolateral (right parasternal-left midaxillary) and anteroposterior (right parasternal-left infrascapular) pad placement in the success of cardioversion. However, a subgroup analysis indicated anterolateral placement might be more effective when using biphasic shocks.29


Managing Atrial Fibrillation Secondary to…

=>Sepsis: Do use BBs

AF is an independent predictor of mortality the critically ill, AF confers 31% mortality versus patients without AF at 17% mortality (P<0.001).30 A retrospective cohort by Walkey et al of 39,693 septic patients with AF analyzed practice patterns and mortality. CCBs were most commonly initiated in AF during sepsis (36%); however, BBs were associated with lower hospital mortality compared to CCB (RR 0.92), digoxin (R 0.79), and amiodarone (RR 0.64).31

=>Hyperthyroid: Do use BBs

BBs are recommended to control AF complicating thyrotoxicosis unless contraindicated (Level C).4 The rationale is two-fold, first hyperthyroidism is a state of increased β -adrenergic receptors thus BB reduce symptoms.32 Second, propranolol, atenolol, and metoprolol slowly decrease serum T3 concentrations by inhibiting the conversion from thyroxine (T4).33, 34

=>Heart Failure: Do use BBs

The AF-CHF study by Dydra et al compared rate versus rhythm control strategies in CHF. The study enrolled 1,376 patients with an EF <35% and recent history of AF, patients were randomized to rate control utilizing BB or rhythm control utilizing electrical cardioversion and amiodarone. Rhythm control was abandoned more frequently than rate control, 21% versus 9.1% respectively. The predominant reason to abandon rate control was worsening heart failure. Importantly, crossover from rhythm to rate control did not increase cardiovascular or all cause mortality.35 Although rate control is an acceptable strategy in CHF, BB therapy does not confer the same mortality benefit in AF as it does in sinus rhythm.36 Therefore, BB can be used in HF but does not need to be the only or first line agent.

The decrease in SVR, anti-ischemic effects, and LV relaxation of CCBs indicate theoretical benefit in CHF. However, the negative inotropic effect may impair left ventricular function.37 Furthermore, the MDPIT study by Goldstein et al showed post-MI patients on CCBs with early LV dysfunction (EF <40%) were found to have increased late onset heart failure.21 Although the evidence is not overwhelming, in cases of rapid AF and CHF, particularly decompensated HF, rate control with CCBs can be detrimental.


Briefly on Antithrombotic Therapy: DO anticoagulate.4,38

Patients with AF greater than 48 hours or less than 48 hours but high risk of stroke and no contraindications for anticoagulation should initiate anticoagulation as soon as possible before or immediately after cardioversion.4


  • Patients with nonvalvular AF, CHA2DS2-VASc is recommended for stroke risk assessment (Level B evidence).4
  • CHA2DS2-VASc39
    • Congestive Heart Failure
    • Hypertension
    • Age >75 (2 points)
    • Diabetes mellitus
    • Prior Stroke or TIA or Thromboembolism (2 points)
    • Vascular disease – prior MI, PAD, aortic plaque
    • Age 65 to 74 years
    • Female Sex
  • Scoring (% risk of stroke/year)
    • 0 No therapy (0%/year)
    • 1 Aspirin 325mg or oral anticoagulants (1.3%/year)
    • ≥2 Oral Anticoagulants recommended (2.2%/year)
      • Warfarin, Dabigatran, Rivaroxaban, Apixaban
    • Anticoagulants
      • Renal function should be assessed in NOACs (Direct thrombin or factor Xa inhibitors)


  • Valve replacement – anticoagulation with warfarin INR 2 to 3 or 2.5 to 3.5 depending on tissue versus mechanical valve selection



  • Do

    • Reverse/treat any underlying process (remember PIRATES)
    • Use β1-selective BBs or non-dihydropyridine CCBs in rapid AF
    • Use BB in patients with concurrent hyperthyroid
    • Use CHA2DS2-VASc to risk stratify for stroke
  • Don’t

    • Mix BB and CCB (if possible)
    • Use a BB in severe asthma
    • Use a CCB in decompensated HF
    • Cardiovert stable AF with duration >48h or unknown duration if the patient isn’t on anticoagulation


References / Further Reading

  1. Hagens VE, Van Gelder IC, Crijns HJ, Group RACVECOPAFS. The RACE study in perspective of randomized studies on management of persistent atrial fibrillation. Cardiac electrophysiology review. 2003;7(2):118-121.
  2. Van Gelder IC, Hagens VE, Bosker HA, Kingma JH, Kamp O, Kingma T, et al. A comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillation. The New England journal of medicine. 2002;347(23):1834-1840.
  3. Wyse DG, Waldo AL, DiMarco JP, Domanski MJ, Rosenberg Y, Schron EB, et al. A comparison of rate control and rhythm control in patients with atrial fibrillation. The New England journal of medicine. 2002;347(23):1825-1833.
  4. January CT, Wann LS, Alpert JS, Calkins H, Cigarroa JE, Cleveland JC, Jr., et al. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and the Heart Rhythm Society. Circulation. 2014;130(23):2071-2104.
  5. Abrams J, Allen J, Allin D, Anderson J, Anderson S, Blanski L, et al. Efficacy and safety of esmolol vs propranolol in the treatment of supraventricular tachyarrhythmias: a multicenter double-blind clinical trial. American heart journal. 1985;110(5):913-922.
  6. Delle Karth G, Geppert A, Neunteufl T, Priglinger U, Haumer M, Gschwandtner M, et al. Amiodarone versus diltiazem for rate control in critically ill patients with atrial tachyarrhythmias. Critical care medicine. 2001;29(6):1149-1153.
  7. Ellenbogen KA, Dias VC, Plumb VJ, Heywood JT, Mirvis DM. A placebo-controlled trial of continuous intravenous diltiazem infusion for 24-hour heart rate control during atrial fibrillation and atrial flutter: a multicenter study. Journal of the American College of Cardiology. 1991;18(4):891-897.
  8. Platia EV, Michelson EL, Porterfield JK, Das G. Esmolol versus verapamil in the acute treatment of atrial fibrillation or atrial flutter. The American journal of cardiology. 1989;63(13):925-929.
  9. Scheuermeyer FX, Grafstein E, Stenstrom R, Christenson J, Heslop C, Heilbron B, et al. Safety and efficiency of calcium channel blockers versus beta-blockers for rate control in patients with atrial fibrillation and no acute underlying medical illness. Academic emergency medicine: official journal of the Society for Academic Emergency Medicine. 2013;20(3):222-230.
  10. Siu CW, Lau CP, Lee WL, Lam KF, Tse HF. Intravenous diltiazem is superior to intravenous amiodarone or digoxin for achieving ventricular rate control in patients with acute uncomplicated atrial fibrillation. Critical care medicine. 2009;37(7):2174-2179; quiz 2180.
  11. Demircan C, Cikriklar HI, Engindeniz Z, Cebicci H, Atar N, Guler V, et al. Comparison of the effectiveness of intravenous diltiazem and metoprolol in the management of rapid ventricular rate in atrial fibrillation. Emergency medicine journal: EMJ. 2005;22(6):411-414.
  12. Fromm C, Suau SJ, Cohen V, Likourezos A, Jellinek-Cohen S, Rose J, et al. Diltiazem vs. Metoprolol in the Management of Atrial Fibrillation or Flutter with Rapid Ventricular Rate in the Emergency Department. The Journal of emergency medicine. 2015;49(2):175-182.
  13. Bailey DG, Carruthers SG. Interaction between oral verapamil and beta-blockers during submaximal exercise: relevance of ancillary properties. Clinical pharmacology and therapeutics. 1991;49(4):370-376.
  14. Johnston DL, Lesoway R, Humen DP, Kostuk WJ. Clinical and hemodynamic evaluation of propranolol in combination with verapamil, nifedipine and diltiazem in exertional angina pectoris: a placebo-controlled, double-blind, randomized, crossover study. The American journal of cardiology. 1985;55(6):680-687.
  15. Zeltser D, Justo D, Halkin A, Rosso R, Ish-Shalom M, Hochenberg M, et al. Drug-induced atrioventricular block: prognosis after discontinuation of the culprit drug. Journal of the American College of Cardiology. 2004;44(1):105-108.
  16. Brubacher JR. Beta-Adrenergic Antagonists. In: Hoffman RS, Howland M, Lewin NA, Nelson LS, Goldfrank LR, editors. Goldfrank’s Toxicologic Emergencies. 10e ed. New York, NY: McGraw-Hill; 2015.
  17. Greefhorst AP, van Herwaarden CL. Comparative study of the ventilatory effects of three beta 1-selective blocking agents in asthmatic patients. European journal of clinical pharmacology. 1981;20(6):417-421.
  18. Self TH, Wallace JL, Soberman JE. Cardioselective beta-blocker treatment of hypertension in patients with asthma: when do benefits outweigh risks? The Journal of asthma : official journal of the Association for the Care of Asthma. 2012;49(9):947-951.
  19. Jang DH, DeRoos F. Calcium Channel Blockers. In: Hoffman RS, Howland M, Lewin NA, Nelson LS, Goldfrank LR, editors. Goldfrank’s Toxicologic Emergencies. 10e ed. New York, NY: McGraw-Hill; 2015.
  20. Materne P, Legrand V, Vandormael M, Collignon P, Kulbertus HE. Hemodynamic effects of intravenous diltiazem with impaired left ventricular function. The American journal of cardiology. 1984;54(7):733-737.
  21. Goldstein RE, Boccuzzi SJ, Cruess D, Nattel S. Diltiazem increases late-onset congestive heart failure in postinfarction patients with early reduction in ejection fraction. The Adverse Experience Committee; and the Multicenter Diltiazem Postinfarction Research Group. Circulation. 1991;83(1):52-60.
  22. Clemo HF, Wood MA, Gilligan DM, Ellenbogen KA. Intravenous amiodarone for acute heart rate control in the critically ill patient with atrial tachyarrhythmias. The American journal of cardiology. 1998;81(5):594-598.
  23. Hou ZY, Chang MS, Chen CY, Tu MS, Lin SL, Chiang HT, et al. Acute treatment of recent-onset atrial fibrillation and flutter with a tailored dosing regimen of intravenous amiodarone. A randomized, digoxin-controlled study. European heart journal. 1995;16(4):521-528.
  24. Van Gelder IC, Groenveld HF, Crijns HJ, Tuininga YS, Tijssen JG, Alings AM, et al. Lenient versus strict rate control in patients with atrial fibrillation. The New England journal of medicine. 2010;362(15):1363-1373.
  25. Bardy GH, Ivey TD, Allen MD, Johnson G, Mehra R, Greene HL. A prospective randomized evaluation of biphasic versus monophasic waveform pulses on defibrillation efficacy in humans. Journal of the American College of Cardiology. 1989;14(3):728-733.
  26. Mittal S, Ayati S, Stein KM, Schwartzman D, Cavlovich D, Tchou PJ, et al. Transthoracic cardioversion of atrial fibrillation: comparison of rectilinear biphasic versus damped sine wave monophasic shocks. Circulation. 2000;101(11):1282-1287.
  27. Grubb NR, Cuthbert D, Cawood P, Flapan AD, Fox KA. Effect of DC shock on serum levels of total creatine kinase, MB-creatine kinase mass and troponin T. Resuscitation. 1998;36(3):193-199.
  28. Rao AC, Naeem N, John C, Collinson PO, Canepa-Anson R, Joseph SP. Direct current cardioversion does not cause cardiac damage: evidence from cardiac troponin T estimation. Heart. 1998;80(3):229-230.
  29. Kirkland S, Stiell I, AlShawabkeh T, Campbell S, Dickinson G, Rowe BH. The efficacy of pad placement for electrical cardioversion of atrial fibrillation/flutter: a systematic review. Academic emergency medicine: official journal of the Society for Academic Emergency Medicine. 2014;21(7):717-726.
  30. Shaver CM, Chen W, Janz DR, May AK, Darbar D, Bernard GR, et al. Atrial Fibrillation Is an Independent Predictor of Mortality in Critically Ill Patients. Critical care medicine. 2015;43(10):2104-2111.
  31. Walkey AJ, Evans SR, Winter MR, Benjamin EJ. Practice patterns and outcomes of treatments for atrial fibrillation during sepsis: A propensity-matched cohort study. Chest. 2015.
  32. Bilezikian JP, Loeb JN. The influence of hyperthyroidism and hypothyroidism on alpha- and beta-adrenergic receptor systems and adrenergic responsiveness. Endocrine reviews. 1983;4(4):378-388.
  33. Perrild H, Hansen JM, Skovsted L, Christensen LK. Different effects of propranolol, alprenolol, sotalol, atenolol and metoprolol on serum T3 and serum rT3 in hyperthyroidism. Clinical endocrinology. 1983;18(2):139-142.
  34. Wiersinga WM, Touber JL. The influence of beta-adrenoceptor blocking agents on plasma thyroxine and triiodothyronine. The Journal of clinical endocrinology and metabolism. 1977;45(2):293-298.
  35. Dyrda K, Roy D, Leduc H, Talajic M, Stevenson LW, Guerra PG, et al. Treatment Failure With Rhythm and Rate Control Strategies in Patients With Atrial Fibrillation and Congestive Heart Failure: An AF-CHF Substudy. Journal of cardiovascular electrophysiology. 2015.
  36. Kotecha D, Holmes J, Krum H, Altman DG, Manzano L, Cleland JG, et al. Efficacy of beta blockers in patients with heart failure plus atrial fibrillation: an individual-patient data meta-analysis. Lancet. 2014;384(9961):2235-2243.
  37. Elkayam U. Calcium channel blockers in heart failure. Cardiology. 1998;89 Suppl 1:38-46.
  38. Moukabary T, Gonzalez MD. Management of atrial fibrillation. The Medical clinics of North America. 2015;99(4):781-794.
  39. Mason PK, Lake DE, DiMarco JP, Ferguson JD, Mangrum JM, Bilchick K, et al. Impact of the CHA2DS2-VASc score on anticoagulation recommendations for atrial fibrillation. The American journal of medicine. 2012;125(6):603 e601-606.


Updates on TIA

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

A 54-year-old male with a history of hypertension, coronary artery disease, and hyperlipidemia presents to the emergency department (ED) with a chief complaint of transient right-sided weakness. The weakness lasted five minutes and then resolved without any residual deficits.

The patient’s exam reveals normal vital signs and normal neurologic exam including cranial nerves, motor, sensory, reflexes, cerebellar, and gait.  His electrocardiogram (ECG) reveals left ventricular hypertrophy. The patient’s head computed tomography (CT) is normal.

What work up and management are indicated for transient weakness? What is the appropriate disposition? This article will address the diagnosis and management of transient ischemic attacks (TIA), transient weakness, and more.

How is TIA defined?

The TIA was once defined as a transient neurologic deficit, due to ischemia, with resolution of symptoms in less than 24 hours. In 2009, the American Heart Association (AHA) redefined the TIA as a ‘brief episode of neurological dysfunction resulting from focal cerebral ischemia not associated with permanent cerebral infarction.’ Importantly, even if a patient has resolved symptoms but has a visible infarct on imaging, he or she should be classified as having a stroke.1 Diagnosing a stroke requires imaging resources, most commonly diffusion–weighted magnetic resonance imaging (DWI). With the new definition of TIA, the annual incidence of stroke has increased, but the number of patients disabled due to stroke has decreased.2

TIAs should be taken seriously. In 2007, Johnston et al. demonstrated that patients with TIAs have a 5% risk of stroke within two days and a 10% risk of stroke within three months after sustaining the initial TIA.1,3 TIAs are thought to precede approximately 14%-23% of acute ischemic strokes (AIS). 4,5 A second study demonstrated similar numbers and also found that symptom duration over 60 minutes, age over 60 years, and increased blood pressure were associated with worse clinical outcomes.6

Is everything that presents as a TIA actually a TIA?

Unfortunately, not every person who presents with a transient focal neurologic deficit actually has a TIA. Atypical migraines, encephalopathy, seizures, neuropathy, psychiatric conditions, and metabolic pathology can all present as mimics of TIA. The literature demonstrates that anywhere between 5% and 31% of patients presenting with stroke-like symptoms actually have alternative diagnoses. Prabhakaran et al. found high rates of misdiagnosing mimics as TIA, with misdiagnosis rates ranging from 30% to 62%.7

Another study by Whiteley et al. found that 1/3 of patients with suspected TIA actually had a TIA mimic.8 Similarly, in a cohort study of 303 patients, approximately 18% of suspected TIA patients actually had experienced a mimic.9 Unfortunately, this study also found patients with TIA and mimics to have similar rates of vascular comorbidities, blood pressures upon arrival, duration of symptoms, aphasia, dysarthria, vertigo, unilateral sensory loss, and hemianopia.9 This can most certainly make diagnosing an actual TIA more difficult. The authors did find, however, that memory loss, headache, and blurred vision were associated with mimics, while unilateral weakness was more associated with true TIA.

Is imaging helpful in diagnosing TIA?

Unfortunately, this is complicated. A 2012 study by Förster et al evaluated imaging techniques in patients with symptoms concerning for acute TIA. The authors found that within the first 24 hours of symptoms, imaging is not perfect. CT rarely demonstrates acute ischemic findings. In the same 2012 study, 95.7% of scans were found to be normal and only 4.3% showed possible infarction.  Magnetic resonance imaging (MRI) was found to be somewhat better, demonstrating 35% of acute infarcts.10 If possible, MRI with diffusion-weighted imaging (DWI) should be obtained, as it is more sensitive than CT for detecting acute ischemia, prior bleeding, and other lesions.11,12 MRI can also be helpful in these patients as those with DWI abnormalities are at high risk for stroke no matter their prognostic score (see below).13

Doppler ultrasound (US), CT angiography, and magnetic resonance angiography (MRA) comprise further options for vascular imaging. Carotid Doppler US is often used to evaluate for carotid stenosis, where greater than 50% stenosis warrants consideration for further treatment.1

Are scoring systems helpful?

One big question regarding stroke care is whether one can predict who will experience a stroke following a TIA. The assumed risk of stroke within 90 days following a TIA is approximately 10%. Several scoring systems to help predict possible stroke are available.  The ABCD2 score is perhaps the most well-known.  Unfortunately, this score does not take imaging into account.

ABCD2 picture


Diagram http://image.slidesharecdn.com/chadabcdscore-111029024736-phpapp02/95/chads2-and-abcd-score-2-728.jpg?cb=1319856502

We are classically taught using the ABCD2 score will adequately predict stroke risk. However, recent literature questions the predictive value of this score.  In 2011, Perry et al. conducted an external validation of the ABCD2 and found that by using this score, physicians may misclassify up to 8% of patients as low risk. Additionally, the sensitivity of the score for high risk patients was found to be only 31.6%.14 Stead et al. compared the ABCD2 score to brain and carotid imaging for risk stratification and found the ABCD2 score to provide no useful additional information.15 Schrock et al. found the  ABCD2score to be unhelpful toward guiding diagnostic testing, as 15% of patients with high grade carotid stenosis would be missed if ABCD2 was used alone.16  An Australian study also assessed use of the ABCD2 score in the ED and found the ABCD2 to have poor predictive value toward determining future stroke. Those patients who were calculated as low, moderate, and high risk on the ABCD2 all had similar rates of stroke at 30 and 90 days (around 1% at 30 days and 2% at 90 days).17 An Annals of Emergency Medicine study in 2013 conducted a meta-analysis of the ABCD2 score and found it to be suboptimal in reliably predicting future stroke.18

Hence, the use of the ABCD2 score is questionable for predicting risk of future stroke. Therefore, a 2014 Japanese study modified the score and produced the ABCD3-I score.19 The third D stands for “dual TIA,” or a second TIA episode within one week of the first TIA. The “I” component refers to any abnormal magnetic resonance imaging and/or carotid stenosis greater than 50%.   The study found that dual TIA and carotid stenosis were associated with higher stroke risk, but abnormal MRI imaging was not. Unfortunately, the modified score did not even reach moderate prediction capabilities (C-statistic of 0.66 for ABCD3-I), but it did fare better than the original score (C-statistic of 0.54 for ABCD2). 19

Currently, scoring systems should not take the place of clinical gestalt. They can assist providers in evaluating for risk factors, but they cannot definitively stratify patients into clear-cut categories.

What is the disposition?

The current literature indicates that predicting future stroke risk in patients with TIAs is difficult.  Most would argue that urgent evaluation, risk stratification, and preventative therapy are needed for these patients. Controversy does exist regarding the need for admission, but fortunately, the American Heart Association (AHA) and the National Stroke Association (NSA) have developed certain admission criteria that can be helpful when determining a patient’s disposition needs.

AHA: ABCD2 score of > 3, ABCD2 score of 0-2 and uncertain follow up, or ABCD2 score of 0-2 and evidence that focal ischemia occurred.1

NSA: Consider admission if first TIA within 24-48 hours. For recent TIA within one week, hospitalization is needed for worsening TIA symptoms, duration of symptoms longer than one hour, internal carotid stenosis greater than 50% with symptoms, known cardiac source of embolus, or hypercoagulable state.20

Also, when determining disposition, local resources and patient population should be considered. Difficulty in obtaining follow up and unclear follow up also suggest need for admission.

In patients for whom follow up can be obtained with none of the above high risk factors, acute clinics, rapid evaluation units, or observation units have shown promise.  One study found that patients with follow up within one day demonstrated a 90 day stroke reduction of 8%.21  ED observation units may reduce cost, shorten length of stay, and adequately risk stratify TIA patients in association with neurology consultation.22

Rapid evaluation units

The EXPRESS (Effect of urgent treatment of transient ischemic attack and minor stroke on early recurrent stroke) study conducted in the UK evaluated the use of TIA clinics versus primary care management in patients not admitted to the hospital. Not surprisingly, risk stratification and treatment were faster in the TIA clinic, as well as a significant reduction in stroke from 10% to 2%.21 A study evaluating the use of a round-the-clock TIA clinic called the SOS-TIA clinic, evaluated 1085 patients in a hospital-based clinic, finding a 90 day stroke rate of 1.24% in clinic patients.23  Another study conducted in Germany evaluated outcomes in patients with TIA treated in outpatient clinics that specialize in workup.24  The clinic was staffed by neurologists, and each patient received a MRI or head CT, a carotid US, an ECG, and ankle-brachial indices (ABI). The authors of this study found the stroke rate at 90 days to be 1.6% overall, with 2.9% in the population experiencing TIA or minor stroke. Similarly, a Canadian study found a decreased risk of stroke at 90 days by using the ABCD2 score in conjunction with testing such as carotid US and brain imaging at an outpatient stroke prevention clinic.25   Other studies have shown similar results, with rapid access to a specialized clinic/unit that can risk stratify, properly image, and treat patient comorbidities to reduce stroke risk, but they may result in higher costs.25-27

A dedicated TIA unit, whether TIA clinic or ED observation unit with expedited workup, can reduce recurrent events and need for hospitalization. Studies with these units have found 90 day rates of recurrent events ranging from 1.7% to 3.2%.20,23,27-29

How should patients be managed?

Cornerstones of treatment for TIA revolve around reducing the risk of future events with blood pressure control, lipid control, and antiplatelet agents.1,20,23,30-32 Blood pressure should be maintained at 140/90 with a thiazide diuretic and/or an ACE inhibitor. Statins should be given to keep LDL of under 100mg/dL or 70mg/dL in high risk patients. Niacin or gemfibrozil are recommended to maintain HDL above 40mg/dL. Antiplatelet agents include aspirin with or without dipyridamole, or clopidogrel alone. 33

Multiple studies have evaluated the most efficacious antiplatelet regimen, whether mono or dual therapy. Dual antiplatelet therapy is commonly administered to patients with acute coronary syndromes; however, it is controversial in TIA.  An Australian study found aspirin reduced the absolute risk of stroke in high-risk patients from 7% to 6.1%, with a number needed to treat (NNT) of 110. The addition of clopidogrel produced another 0.5% absolute reduction in stroke, with a NNT of 200.32 Diener et al. found no difference between clopidogrel and aspirin in low risk patients, but clopidogrel was superior in high-risk patients (diabetes, cardiac disease, prior stroke or MI, hyperlipidemia). However, a higher bleeding risk was found in dual therapy.33

In 2013, the CHANCE (Clopidogrel in High-risk patients with Acute Nondisabling Cerebrovascular Events) trial found a 1.4% stroke reduction in patients who used combination therapy (aspirin 75mg daily and clopidogrel 75mg daily). No increased bleeding risk was found. However, aspirin was also provided at only 75mg, as compared to 325mg in other studies.34 Additionally, the study population was predominantly Chinese, which is an important aspect as the Chinese population generally has higher rates of cerebrovascular attacks (CVA), prior CVAs and TIAs, and higher smoking rates than patients in the United States. Later in 2013, Wong et al. conducted a meta-analysis of 14 randomized controlled trials (RCTs), and also included the original CHANCE study.  The authors compared multiple medication regimens and found dual antiplatelet therapy with clopidogrel and aspirin to be associated with decreased stroke risk (relative risk of 0.69), without significantly increasing bleeding risk. Aspirin and dipyridamole were not associated with any risk reduction.35

Other studies including CHARISMA (Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Management, and Avoidance), SPS3, and MATCH trials found no statistical difference between mono-therapy and dual-therapy in reducing future events, but an increased rate of bleeding with dual therapy. 36-38 More recent meta-analyses suggest early treatment with dual therapy within 24 hours of the event may reduce risk of future events, but this should not be extended past 21 days.39,40 Currently, there is insufficient evidence in American populations to recommend clopidogrel plus aspirin, and guidelines from the AHA and NSA should be followed. The ongoing POINT (Platelet Oriented Inhibition in new TIA and minor ischemic stroke) trial is being conducted in the U.S. evaluating clopidogrel with aspirin and aspirin monotherapy.41 

Future Treatments

Medications currently under investigation include cilostazol (predominantly studied in Japan),42 ticagrelor,43 and the new oral anticoagulants. Apixaban, dabigatran, edoxaban, and rivaroxaban may play a future role in prevention of recurrent events.44-49

Other therapies

Cardioembolic TIA is a different animal in that stroke prophylaxis also requires anticoagulant medications. Atrial fibrillation with TIA requires warfarin with a goal INR of 2-3. Anticoagulation is also recommended in the setting of acute myocardial infarction with left ventricular thrombus, dilated cardiomyopathy, or valvular disease.1,20,31

If a major intracranial artery has stenosis of 50%-99%, angioplasty or stent placement may be needed in association with aspirin, blood pressure management, and lipid control. 1,20,31

Bonus: What is the updated 2015 ACEP Clinical Policy on acute ischemic stroke (AIS)?

 1. Is intravenous (IV) tissue plasminogen activatior (tPA) safe and effective for acute ischemic stroke patients if given within 3 hours of symptoms onset?50

Level A: none.

Level B: IV tPA should be offered and may be given to select patients with acute ischemic stroke. The increased risk of symptomatic intracerebral hemorrhage (sICH) should be considered.

Level C: shared decision making when feasible.

  1. Is IV tPA safe and effective for acute ischemic stroke patients treated between 3 to 4.5 hours after symptom onset?

Level B: Despite the known risk of spontaneous intracranial hemorrhage (sICH) and the variability in the degree of benefit in functional outcomes, IV tPA may be offered and given to carefully selected AIS patients within 3 to 4.5 hours after symptom onset at institutions where systems are in place to safely administer the medication.

The policy lists a NNT of 8 for excellent functional outcome if tPA is given within 3 hours of symptom onset and a NNH of 17 for symptomatic intracerebral hemorrhage.

 References / Further Reading

  1.  Easton JD, Saver JL, Albers GW, et al. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease. The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists. Stroke 2009; 40 (6): 2276-93.
  2. Chalela JA, Kidwell CS, Nentwich LM, et al. Magnetic resonance imaging and computed tomography in emergency assessment of patients with suspected acute stroke: a prospective comparison. Lancet. 2007;369(9558):293-298.
  3. Whiteley WN, Wardlaw JM, Dennis MS, Sandercock PA. Clinical scores for the identification of stroke and transient ischaemic attack in the emergency department: a cross-sectional study. J Neurol Neurosurg Psychiatry. 2011 Sep;82(9):1006-10.
  4. Amort M, Fluri F. Transient ischemic attack versus transient ischemic attack mimics: frequency, clinical characteristics and outcome. Cerebrovasc Dis. 2011;32(1):57-64.
  5. Förster A, Gass A. Brain imaging in patients with transient ischemic attack: a comparison of computed tomography and magnetic resonance imaging. Eur Neurol. 2012;67(3):136-41.
  6. Perry JJ, Sharma M. Prospective validation of the ABCD2 score for patients in the emergency department with transient ischemic attack. CMAJ. 2011 Jul 12;183(10):1137-45.
  7. Stead LG, Suravaram S. An assessment of the incremental value of the ABCD2 score in the emergency department evaluation of transient ischemic attack. Ann Emerg Med. 2011 Jan;57(1):46-51.
  8. Schrock JW, Victor A, Losey T. Can the ABCD2 risk score predict positive diagnostic testing for emergency department patients admitted for transient ischemic attack? Stroke. 2009 Oct;40(10):3202-5.
  9. Ghia D, Thomas P. Low positive predictive value of the ABCD2 score in emergency department transient ischaemic attack diagnoses: the South Western Sydney transient ischaemic attack study. Intern Med J. 2012 Aug;42(8):913-8.
  10. Kiyohara T1, Kamouchi M. ABCD3 and ABCD3-I scores are superior to ABCD2 score in the prediction of short- and long-term risks of stroke after transient ischemic attack. Stroke. 2014 Feb;45(2):418-25.
  11. Rothwell PM, Giles MF, Chandratheva A, et al. Effect of urgent treatment of transient ischaemic attack and minor stroke on early recurrent stroke (EXPRESS study): a prospective population-based sequential comparison. Lancet. 2007; 370(9596):1432-1442.
  12. Lavalle ́e P, Meseguer E, Abboud H, et al. A transient ischaemic attack clinic with round-the-clock access (SOS-TIA): feasibility and effects. Lancet Neurol. 2007;6(11):953-960.
  13. Hörer S, Schulte-Altedorneburg G, Haberl RL. Management of patients with transient ischemic attack is safe in an outpatient clinic based on rapid diagnosis and risk stratification. Cerebrovasc Dis. 2011;32(5):504-10.
  14. Wasserman J, Perry J, Dowlatshahi D, et al. Stratified, urgent care for transient ischemic attack results in low stroke rates. Stroke. 2010;41(11):2601-2605.
  15. Wu CM, Manns BJ, Hill MD, Ghali WA, Donaldson C, Buchan AM. Rapid evaluation after high-risk TIA is associated with lower stroke risk. Can J Neurol Sci. 2009 Jul; 36(4):450-5.
  16. Olivot JM, Wolford C, Castle J, et al. Two ACES: transient ischemic attack work-up as outpatient assessment of clinical evaluation and safety. Stroke. 2011;42(7):1839-1843.
  17. Sanders LM, Srikanth VK, Jolley DJ, et al. Monash transient ischemic attack triaging treatment: safety of a transient ischemic attack mechanism-based outpatient model of care. Stroke. 2012; 43(11):2936-2941.
  18. Asimos AW, Johnson AM, Rosamond WD, et al. A multicenter evaluation of the ABCD2 score’s accuracy for predicting early ischemic stroke in admitted patients with TIA. Ann Emerg Med. 2010;55(2):201-210.
  19. Diener HC, Bogousslavsky J, Brass LM, et al. Aspirin and clopidogrel compared with clopidogrel alone after recent ischaemic stroke or transient ischaemic attack in high-risk patients (MATCH): randomised, double-blind, placebo-controlled trial. Lancet. 2004;364(9431):331-337.
  20. Bhatt DL, Fox KA, Hacke W, et al. Clopidogrel and aspirin versus aspirin alone for the prevention of atherothrombotic events. N Engl J Med. 2006;354(16):1706-1717.
  21. SPS3 Investigators; Benavente OR, Hart RG, McClure LA, Szychowski JM, Coffey CS, Pearce LA. Effects of clopidogrel added to aspirin in patients with recent lacunar stroke. N Engl J Med. 2012;367(9):817-825.
  22. Diener HC, et al. Aspirin and clopidogrel compared with clopidogrel alone after recent ischaemic stroke or transient ischaemic attack in high-risk patients (MATCH): randomised, double-blind, placebo-controlled trial. The Lancet. 2004. 364(9431):331-337.
  23. Lee M, Saver J, Hong KS, Rao NM, Wu YL, Ovbiagele B. Risk- benefit profile of long-term dual- versus single-antiplatelet therapy among patients with ischemic stroke: a systematic review and meta-analysis. Ann Intern Med. 2013;159(7):463-470.
  24. Shinohara Y, Katayama Y, Uchiyama S, et al. Cilostazol for prevention of secondary stroke (CSPS 2): an aspirin-controlled, double-blind, randomised non-inferiority trial. Lancet Neurol. 2010;9(10):959-968.
  25. SOCRATES trial. Web site. http://www.clinicaltrials.gov/show/ NCT01994720. Accessed September 1, 2014.
  26. Granger CB, Alexander JH, McMurray JJ, et al. Apixaban versus warfarin in patients with atrial fibrillation. N Engl J Med. 2011; 365(11):981-992.
  27. Connolly SJ, Eikelboom J, Joyner C, et al. Apixaban in patients with atrial fibrillation. N Engl J Med. 2011;364(9):806-817.
  28. Connolly SJ, Ezekowitz MD, Yusuf S, et al. Dabigatran versus warfarin in patients with atrial fibrillation. N Engl J Med. 2009;361(12):1139-1151.
  29. Giugliano RP, Ruff CT, Braunwald E, et al. Edoxaban versus warfarin in patients with atrial fibrillation. N Engl J Med. 2013;369(22):2093-2104.
  30. Patel MR, Mahaffey KW, Garg J, et al. Rivaroxaban versus warfarin in nonvalvular atrial fibrillation. N Engl J Med. 2011;365(10):883-891.
  31. Diener HC, Eikelboom J, Connolly SJ, et al. Apixaban versus aspirin in patients with atrial fibrillation and previous stroke or transient ischaemic attack: a predefined subgroup analysis from AVERROES, a randomised trial. Lancet Neurol. 2012;11(3): 225-231.
  32. Clinical Policy: Use of Intravenous tPA for the Management of Acute Ischemic Stroke in the Emergency Department. Ann Emerg Med. http://www.acep.org/workarea/DownloadAsset.aspx?id=89978
  33. Diener HC, Bogousslavsky J, Brass LM, et al. Aspirin and clopidogrel compared with clopidogrel alone after recent ischaemic stroke or transient ischaemic attack in high-risk patients (MATCH): randomised, double-blind, placebo-controlled trial. Lancet. 2004;364(9431):331-337.
  34. Bhatt DL, Fox KA, Hacke W, et al. Clopidogrel and aspirin versus aspirin alone for the prevention of atherothrombotic events. N Engl J Med. 2006;354(16):1706-1717.
  35. SPS3 Investigators; Benavente OR, Hart RG, McClure LA, Szychowski JM, Coffey CS, Pearce LA. Effects of clopidogrel added to aspirin in patients with recent lacunar stroke. N Engl J Med. 2012;367(9):817-825.
  36. Diener HC, et al. Aspirin and clopidogrel compared with clopidogrel alone after recent ischaemic stroke or transient ischaemic attack in high-risk patients (MATCH): randomised, double-blind, placebo-controlled trial. The Lancet. 2004. 364(9431):331-337.
  37. Lee M, Saver J, Hong KS, Rao NM, Wu YL, Ovbiagele B. Risk- benefit profile of long-term dual- versus single-antiplatelet therapy among patients with ischemic stroke: a systematic review and meta-analysis. Ann Intern Med. 2013;159(7):463-470.
  38. Shinohara Y, Katayama Y, Uchiyama S, et al. Cilostazol for prevention of secondary stroke (CSPS 2): an aspirin-controlled, double-blind, randomised non-inferiority trial. Lancet Neurol. 2010;9(10):959-968.
  39. SOCRATES trial. Web site. http://www.clinicaltrials.gov/show/ NCT01994720. Accessed September 1, 2014
  40. CB, Alexander JH, McMurray JJ, et al. Apixaban versus warfarin in patients with atrial fibrillation. N Engl J Med. 2011; 365(11):981-992.
  41. Connolly SJ, Eikelboom J, Joyner C, et al. Apixaban in patients with atrial fibrillation. N Engl J Med. 2011;364(9):806-817.
  42. Connolly SJ, Ezekowitz MD, Yusuf S, et al. Dabigatran versus warfarin in patients with atrial fibrillation. N Engl J Med. 2009;361(12):1139-1151.
  43. Giugliano RP, Ruff CT, Braunwald E, et al. Edoxaban versus warfarin in patients with atrial fibrillation. N Engl J Med. 2013;369(22):2093-2104.
  44. Granger CB, Alexander JH, McMurray JJ, et al. Apixaban versus warfarin in patients with atrial fibrillation. N Engl J Med. 2011; 365(11):981-992.
  45. Connolly SJ, Eikelboom J, Joyner C, et al. Apixaban in patients with atrial fibrillation. N Engl J Med. 2011;364(9):806-817.
  46. Connolly SJ, Ezekowitz MD, Yusuf S, et al. Dabigatran versus warfarin in patients with atrial fibrillation. N Engl J Med. 2009;361(12):1139-1151.
  47. Giugliano RP, Ruff CT, Braunwald E, et al. Edoxaban versus warfarin in patients with atrial fibrillation. N Engl J Med. 2013;369(22):2093-2104.
  48. Patel MR, Mahaffey KW, Garg J, et al. Rivaroxaban versus warfarin in nonvalvular atrial fibrillation. N Engl J Med. 2011;365(10):883-891.
  49. Diener HC, Eikelboom J, Connolly SJ, et al. Apixaban versus aspirin in patients with atrial fibrillation and previous stroke or transient ischaemic attack: a predefined subgroup analysis from AVERROES, a randomised trial. Lancet Neurol. 2012;11(3): 225-231.
  50. Clinical Policy: Use of Intravenous tPA for the Management of Acute Ischemic Stroke in the Emergency Department. Ann Emerg Med. http://www.acep.org/workarea/DownloadAsset.aspx?id=89978

Identifying Complete Heart Block and the use of Temporary Cardiac Pacing in the Emergency Department

Authors: Katherine Stolper, DO (EM Resident at SAUSHEC, USA) and Brit Long, MD (@long_brit, EM Chief Resident at SAUSHEC, USAF) // Edited by: Jennifer Robertson, MD, MSEd and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

Case Presentation

You are working in the emergency department (ED) when you overhear the emergency medical services (EMS) report of an incoming 89 yo female with chief complaint of “fall from standing” with no apparent injuries.  She is presenting to your ED as a trauma resuscitation secondary to a brief episode of unresponsiveness in the ambulance. Her unresponsiveness resolved with four chest compressions.

Upon arrival, she has a Glasgow Coma Scale (GCS) of 15 with her airway, breathing and circulation intact. Her initial vital signs are heart rate (HR) 56, blood pressure (BP) 176/72, respiratory rate (RR) 20, oxygen saturation 97% on room air (RA), temperature 98.1°F, and glucose of 89.

ECG Pic 1

The primary and secondary surveys are unremarkable. However, while the patient is waiting for a computed tomography (CT) scan, her monitor demonstrates several seconds of asystole. She becomes unresponsive but has rapid return of circulation after a sternal rub.

The electrocardiogram (ECG) above shows a third degree (complete) atrioventricular (AV) block. This article will review third degree AV blocks and their management.


Complete AV block is a complete dissociation between the atria and the ventricles. This means that the electrical impulses generated in the atria do not propagate to the ventricles.  An ECG will show P waves and QRS complexes that are independent of each other, as seen in the ECG.  Since none of the atrial impulses are propagating, you will see an escape rhythm that is either junctional (rate 40-60 beats per minute (bpm) or ventricular (rate 20-40 bpm) depending on the level of the block.  Of note, junctional escape rhythms tend to be more stable than ventricular escape rhythms. The etiologies of complete heart block include both reversible and irreversible causes but the most common cause is coronary ischemia.

Reversible Causes Irreversible Causes
-Medications: Calcium channel blockers, Beta blockers, Amiodarone, Adenosine, Digitalis -Idiopathic degeneration of the conducting system – Lenegre’s or Lev’s disease
-Hyperkalemia -Congenital – maternal lupus
-Inferior Myocardial Infarction -Amyloidosis/Sarcoidosis
-Increased vagal tone -Lyme disease
-Hypothyroidism -Structural defect: Myocardial infarction (anterior), heart failure
-Heart valve surgeries

Is atropine indicated in bradycardic patients with complete heart block?

According to the American Heart Association (AHA) Advanced Cardiac Life Support (ACLS) guidelines, atropine is indicated as a first line agent for patients with unstable bradycardia. It works by inhibiting vagal stimulation.  Atropine is given as 0.5mg intravenously (IV) every 3-5 minutes with a maximum dose of 3 mg. Atropine administration, however, should not interfere with cardiac pacing.  If there is a favorable response to atropine, the conduction abnormality is likely in the AV node. However, if the escape rhythm is originating at or below the bundle of His, there is unlikely to be a response to atropine as the more distal conducting system is not as sensitive to vagal stimulation. [1,2]

Response to atropine can be predicted by looking at the QRS morphology on a 12 lead ECG.  If the AV block occurs in the AV node or the Bundle of His, the escape rhythm will have a narrow QRS and will likely respond to atropine. Conversely, if the AV block occurs below the bundle of His, the escape rhythm results in a sub-junctional escape rhythm which has a wide QRS and is unlikely to respond to atropine [3].

NOTE: Because atropine can increase cardiac demand, it is contraindicated in patients with complete heart block secondary to myocardial infarction or ischemia.

Titrating to patient response, epinephrine (2-10 mcg/min) or dopamine (2-10 mcg/kg/min) should be considered while waiting for a pacemaker or if pacing is ineffective.


The two types of temporary cardiac pacing that you will encounter in the ED are transcutaneous and transvenous. Temporary cardiac pacing is indicated for patients with symptomatic bradycardic dysrhythmias, most frequently due to AV nodal block. [7] Remember that bradycardia is not always due to primary cardiac issues such as sick sinus syndrome, atrioventricular block, or myocardial ischemia. Always consider secondary causes of bradycardia such as hyperkalemia, hypothyroidism, hypothermia, or overdose with beta-blockers, calcium channel blockers, digitalis, clonidine, or other antiarrhythmics.

Transcutaneous Pacing

Transcutaneous pacing is a great option for an unstable patient in whom central venous access has not been established yet for a transvenous pacemaker.  Unfortunately, patient discomfort and high pacing thresholds are significant clinical barriers to transcutaneous pacing. Patient discomfort is secondary to skeletal muscle contraction, however, research shows that less electricity can be used due to the newer technology available with larger surface area pads. With the new technology, most patients can tolerate > 15 minutes of transcutaneous pacing [5]. However, in patients who cannot tolerate it, sedation and analgesia can be provided to mitigate any discomfort.


  1. Pad Placement and set up: Recommended pad placement for the best capture is anterior/posterior, as shown below. The positive pad is placed posteriorly to the left of the spine, beneath the left scapula. The negative pad is placed anteriorly between the xiphoid process and the left nipple.

Pic 2 Pad Placement

Alternatively, the pads may both be placed anteriorly, with the negative electrode placed in the V6 position and the positive electrode to the right of the sternum, under the clavicle.

Pic 3 Pad Placement

  1. Select Mode: Select the pacemaker button on the box and choose between fixed and demand modes. Fixed mode means that the pacemaker will fire at whatever rate you choose, regardless of the patient’s intrinsic rhythm. Demand mode will sense the patient’s intrinsic rhythm and pace only if needed. Most often you will start in fixed mode.
    • NOTE: If in demand mode, the leads should be placed for continuous ECG so that the pacemaker can sense the patient’s intrinsic rate to pace accordingly (double set up). This prevents the “R on T” phenomenon.
  1. Set rate and output: The initial pacing rate should be set to 80 bpm with the current set to 30 milliamperes (mA). Beware that initially, pacemaker spikes may be visualized without resultant cardiac depolarization.

 The current can be increased by 5-10 mA at a time until capture is seen as a definite QRS complex and T wave following each pacemaker spike.  Once capture is achieved, check the patient’s pulse or correlate with the pulse oximeter to ensure that a perfusing rhythm is present.[8]  Final output should be set to 5-10 mA above threshold level to ensure continued capture.

Human studies have shown that the average current necessary to achieve capture is between 65-100 mA in unstable bradycardias and about 50-70 mA in hemodynamically stable patients. [5]

Transvenous Pacing

There are no absolute contraindications to transvenous pacing. However, some relative contraindications to transvenous pacing include: patients with mild or rare intermittent symptoms with a stable escape rhythm, patients with prosthetic tricuspid valves, and patients with myocardial infarctions who are receiving thrombolytic agents or aggressive anti-platelet therapy.

NOTE: Also use caution in patients with digitalis toxicity as the myocardium is extremely sensitive to irritation from the transvenous wire and can cause the rhythm to degenerate into ventricular fibrillation.


  • Venous sheath (6 French (Fr))
  • Pacing wire/catheter
  • Pacing generator
  • Extension cable
  • Sterile precautions


  1. Achieve Access: Insert a 6 Fr catheter. Note the internal diameter of the catheter sheath needs to match the external diameter of the pacemaker wire. Most balloon tip catheters are 5 Fr and will fit into a 6 Fr catheter. The ideal site selection for the venous catheter is the right internal jugular vein or the left subclavian vein, as these veins give you the most direct route to the right ventricle.
  1. Hook up your pacing generator: Put a fresh battery in the generator (usually a 9 volt (V) battery) and turn it on. There will be an extension cable with the connector terminals, and the pacing catheter with two electrode connectors at the end. The electrode connectors will need to be connected to the 2 terminals. The proximal (positive) electrode on the catheter plugs into the positive connector terminal and the distal (negative) electrode plugs into the negative connector terminal. You can remember this as “PP” for “Positive Proximal.” Finally, plug the extension cable into the top of the generator box.

Note: If you have a dual chamber pacemaker, make sure it is plugged into the ventricular port.


Pic 4 leftPic 5 Right

  1. Initial pacemaker settings: As shown above, there are three things that need to be set on your generator. These include rate, output, and sensitivity.
  • Rate: Rate should be set above the patient’s native rate and above the rate of your transcutaneous pacemaker Set pacing at 80-100 bpm initially so it is easy to tell when capture is obtained, and then turn the rate down to approximately 60 bpm to avoid demand ischemia after capture has been confirmed.
  • Output: This is the amount of current that is being sent to the heart and is measured in mA. This is initially set to the maximum which will usually be 20 mA. Note: If pacing is dual chamber, atrial output should be set to zero mA and ventricular output to maximum mA.
  • Sensitivity This is the pacemaker’s ability to see the electrical activity coming from the heart as measured in millivolts (mV). The lower the sensitivity number, the more sensitive the pacemaker is at detecting intrinsic cardiac activity.Pic 6 mV
  • Start with the sensitivity set to “asynchronous” which means the generator will fire at the set rate, no matter what the intrinsic activity of the heart is.  This makes it easier to determine once capture occurs.Once you have capture, you can switch to synchronous (or demand) mode.  This avoids the “R on T” phenomenon. To find the sensitivity threshold, turn down the rate below the patient’s intrinsic rate and start with the sensitivity dial on the lowest number. Dial up until the pacemaker fails to sense any activity and starts firing. The sensitivity threshold is usually more than 5 mV.  The sensitivity setting should be half the sensitivity threshold, meaning the pacemaker should be twice as sensitive as the sensitivity threshold.
    • Insert the pacing catheter and determine capture:
      • Inflate the balloon once it is at least 20 cm inserted (to ensure it is past the end of the catheter), turn the stopcock to ensure the balloon stays inflated, and advance the wire. The balloon works like a sail to guide the wire into the right ventricle (RV). Make sure to use the 1.5 ml syringe that comes in the kit to avoid overinflating the balloon.
      • Running IV fluids through the catheter while floating the wire can also help guide the balloon into the RV.
      • Ideal placement of the catheter should be at a depth of approximately 40-45cm.
      • Ultrasound guidance using either a parasternal long or subxiphoid view can be helpful to visualize the catheter tip in the RV.
      • If you overshoot and need to pull back the wire, make sure the balloon is deflated to avoid tearing the tricuspid valve leaflets
      • Once you achieve capture, pacemaker spikes will become apparent and will be soon followed by a widened QRS. This will have a similar appearance to a left bundle branch block as the electrode contacts the wall of the RV. Make sure you check a pulse to ensure that you have a perfusing rhythm. You can also use the pulse oximetry to correlate the QRS complexes with a pulse.
      • Deflate the balloon, decrease the output until you lose capture then double the output, typically between 1-5 mA.
      • Obtain a chest x-ray for placement confirmation.


    PEARL: Defibrillation and cardioversion are safe in patients who have temporary pacemakers.


    1. Failure to Pace/Output failure – The pacemaker does not produce a stimulus when it shuld. Check your wire connections and the battery in the pacemaker box. Check for breaks or kinks in the wires. To exclude other causes, turn the sensitivity to asynchronous and the output to maximum

    Switch back to transcutaneous pacing until a new wire can be floated

    .Failure to Pace Output Failure
    2. Undersensing (risk of R on T) – The pacemaker fires with no regard for the patient’s intrinsic rhythm. Turn down the sensitivity. Remember the lower the number the more sensitive the pacemaker is.Undersensing

    3. Oversensing (risk of failure to pace) – the pacemaker thinks it detects an intrinsic QRS and inhibits itself from firing. This is common with skeletal muscle contraction from shivering or seizures or from a tall T wave. To solve this,  turn up the sensitivity to make the pacemaker less sensitive. Also turn the pacemaker to asynchronous.Oversensing

    4. Failure to Capture – You will see pacemaker spikes with no associated QRS complex as in the figure below Turn up the current until you regain capture, check for electrolyte abnormalities, reposition the wire or roll the patient from one side to anothe, or try changing the polarity – which wire is in the positive and negative port.Failure to Capture


    References / Further Reading

    1. “ACLS Drugs for Bradycardia.” ACLS Algorithms. Web. Nov.-Dec. 2015
    2. Link, M. S., D. L. Atkins, R. S. Passman, et al. “Part 6: Electrical Therapies: Automated External Defibrillators, Defibrillation, Cardioversion, and Pacing * 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.” Circulation 122.18_suppl_3 (2010): S706-S719
    3. Saure, William, et. al. “Third degree (complete) atrioventricular block” UptoDate. Web 18 Nov 2015
    4. Neumar RW, Otto CW, Link MS, et al. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010; 122:S729.
    5. Boehm, Judy. “Tried and True: Noninvasive Cardiac Pacing.” Zoll. N.p., n.d Web. Nov.-Dec. 2015
    6. Flower, Oliver. “Temporary Pacemakers in Critical Care.” Intensive Care Network. N.p., 20 Aug. 2015. Web. 10 Dec. 2015.
    7. Hayes, David. et.al. “Temporary cardiac pacing” UptoDate. Accessed 07Dec15
    8. Deal, Nathan, et. al “Focus On: Transcutaneous and Transvenous cardiac pacing. American College of Emergency Physicians. Web. 12 Dec. 2015
    9. Wood, Mark A., and Kenneth A. Ellenbogen. “Temporary Cardiac Pacing.” Cardiac Pacing and ICDs (2005): 163-95. University of Ottawa Heart Institute. Web. 20 Dec. 2015.