EKG of the Week 2017 4-16

This EKG comes courtesy of Dr. Altberg.

A 19 year old male presents to the ED intoxicated. He also complains of palpitations. His EtOH level is 261. (This is equivalent to a blood alcohol content of 0.26).

His vital signs are: Pulse 140, Respirations 18, BP 120/80.

His EKG is below.

1.       What does the EKG demonstrate?

2.       How would you manage this patient?


The EKG demonstrates atrial fibrillation. In the setting of acute alcohol intoxication, this is known as Holiday Heart Syndrome.

The heart rate is normal. No specific interventions are necessary. The patient should be observed on telemetry until the a-fib resolves.


Patients who “binge drink” are at risk for supraventricular arrhythmias, with atrial fibrillation being the most common. It can also cause atrial flutter, atrial tachycardia, and PVC’s. These patients are typically healthy with no past history of cardiac disease. When they stop drinking, the symptoms go away. This is known as Holiday Heart Syndrome. The arrhythmias can occur at the time of drinking or up to 36 hours later.

Patients with Holiday Heart Syndrome typically present with palpitations. They may also have chest pain and syncope. There are several mechanisms that have been proposed to explain why Holiday Heart occurs.

Initial treatment of patients with Holiday Heart is the same as other patients with atrial fibrillation. If they are tachycardic, their rate should be controlled with AV nodal blockers. However, they are typically at low risk for clots and usually do not require anticoagulation. Rhythm control is usually unnecessary as the arrhythmia usually resolves spontaneously within 24 hours. They should be admitted to a monitored setting.


(Tonelo, et al. Holiday Heart Syndrome Revisited after 34 Years. Arq Bras Cardiol. 2013 Aug; 101(2): 183–189.)

(Voskoboinik, Alcohol and Atrial Fibrillation : A Sobering Review. Journal of the American College of Cardiology. Volume 68, Issue 23, 13 December 2016, Pages 2567–2576)


Pulmonary Hypertension and Right Ventricular Failure

Mikhail Podlog, DO

Editor: Anna Van Tuyl, MD



The left ventricle (LV) is widely studied and much is known about its normal function, how it performs under stress, and the causes, sequelae, and treatments of LV failure. On the other hand, much less is understood about the right ventricle (RV), including right ventricular failure (1,3). There are many causes of right ventricular failure, the most common being failure of the left ventricle, but one important condition to always consider is pulmonary hypertension (PH), defined as a mean pulmonary artery pressure of 25 mm Hg or higher (1). As pulmonary pressures rise, the increase in afterload on the RV decreases right ventricular stroke volume and output, increasing RV volume.  Since the RV cannot adapt as rapidly as the LV to increases in afterload, this has several detrimental effects on the cardiovascular system.

First, the increased volumes and pressures in the RV causes bulging of the interventricular septum into to LV, decreasing left ventricular preload. This results in a decrease in cardiac output, leading to hypotension and cardiac ischemia (1,3). Second, increased pressures in the RV cause a rise wall tension, decreasing right coronary artery perfusion, which leads to further ischemia. (1,3) Finally, increased pressures in the RV cause tricuspid regurgitation leading to decreased cardiac output (2). All of these processes ultimately cause what is referred to as the right ventricular spiral of death. 



World Health Organization (WHO) Classifications of Pulmonary Hypertension


As always, the first step is considering the diagnosis. The most common presenting complaint is exertional dyspnea and pulmonary hypertension should always be thought about if an alternative diagnosis does not explain the patient’s presentation (1). Although a definitive diagnosis of PH requires right heart catheterization, there are several ways ED providers can assess for its presence.

Cardiac Ultrasound
1.    Apical 4 (A4) chamber – RV greater than 2/3rd-1x the size of LV (1,4)
2.    Parasternal short – flattening of interventricular septum, D-shaped LV (1,2)
3.    TAPSE (Tricuspid Annular Plane Systolic Excursion)- M mode through tricuspid annulus in A4 view, >1.6 nml, <1.0 severe dysfunction (7)

CTA Chest  - If RV is greater than 9/10ths of LV, that correlates with increased risk of adverse events and death. (1,4)


Definitive treatment of pulmonary hypertension usually involves treating the underlying causes. This includes diuretics for left heart failure, bronchodilators and steroids for lung diseases, thrombolysis for pulmonary emboli, etc. Appropriate consultations with cardiologists, pulmonologists and other specialists is also emergently indicated for further management. (1,2,3) In the meantime, there are certain things that emergency department providers must do to resuscitate and stabilize the patient in front of them.

Optimize Volume Status

Volume status in these patients is difficult to assess, as the physical exam as well as ultrasound visualization of the IVC is often unreliable. Overloading these patients can lead to further increase in RV volume causing decreased cardiac output and an accelerated path down the spiral of death. Overly diuresing these patients may also lead to a decreased cardiac output if the patient is preload dependent. Here are some tips one can use to assess these patients. (2)

1.     Assume the patient is fluid overloaded and avoid large boluses of fluids -> negative balance is usually key for these patients. (1,2,6)

2.     If there is clear volume loss (diarrhea, blood loss) -> low volume boluses of 250cc of isotonic solution and monitor for effects on blood pressure, heart rate, and urine output.  (1)

a.     If patient is anemic transfuse blood as decreased Hgb and iron has been associated with increased mortality (3,4)

3.     Use passive leg raise maneuver and assess for changes in blood pressure and heart rate (this stimulates giving a bolus and can be rapidly reversed by lowering the legs).

4.     Consider expedited admission to the ICU where a pulmonary artery catheter can be used to obtain accurate central pressures and guide further fluid management, although the efficacy of this is highly debated. (2)

Consider early pressor support

Systemic vasopressors can help prevent the downward spiral of RV failure several ways. Increasing left ventricular afterload can decrease interventricular septum bowing into the LV, increasing cardiac output. Vasopressors also assist in maintaining coronary perfusion to the right ventricle, decreasing effects of ischemia. Although literature is very scant comparing the variety of pressors available, certain pressors have advantages over others in treating pulmonary hypertension.

1.     Norepinephrine – proven benefits in several types of shock; helps maintain coronary perfusion of right ventricle; may increase pulmonary vascular resistance (1,4)

2.     Vasopressin – peripheral vasopressor just like norepinephrine, may actually decrease pulmonary vascular resistance through a NO-induced mechanism (1,2)

3.     Phenylephrine – avoid due to increase in pulmonary vascular resistance when compared to other pressors available (1,5)

4.     Dobutamine – augments myocardial contractility and reduces RV and LV afterload -> increased CO; but disadvantages include decreased SVR and tachycardia so may need to combine with a vasopressor (1,2,3,4)

5.     Milrinone – Unlike dobutamine, PDE3 inhibitors are inotropic and augment cardiac output without chronotropic effects, but disadvantages include decreased SVR as well so may need to combine with a vasopressor; may consider inhaled milrinone if available (2,3,4)

Treat atrial arrhythmias

Patient with pulmonary hypertension are predisposed to atrial tachyarrhythmias. These patients do not tolerate atrial arrhythmias as cardiac output is preload dependent and any minor change can have drastic effects.  Calcium channel blockers and beta blockers should be avoided as they may further impair cardiac function. Cardioversion should always be strongly considered as first line especially for unstable patients (1). Amiodarone can be tried if the patient is stable, and can also be used to pretreat the patient prior to cardioversion. (2,3)

Pulmonary Vasodilations

Pulmonary vasodilators are the only medications that directly reverse the symptom-causing pathology. These are very useful in patients with idiopathic pulmonary hypertension (Category 1) and must be quickly given if a patient is on an IV pump of these medications that has malfunctioned. Inhaled preparations of these medications are also very effective at delivery the medication to highly ventilated portions of the lung, causing local vasodilation and improving V/Q mismatch. Below is a table that lists the categories of pulmonary vasodilators and their potential uses in emergencies.



Airway and ventilation management

Maintaining tight control of ventilation and oxygenation is crucial in these patients. Hypoxemia as well as hypercarbic respiratory acidosis can lead to increased pulmonary vasoconstriction, further exacerbating the underlying pathology. Therefore oxygen saturations and carbon dioxide levels in the blood must be maintained in the normal range. (1,4)

If a patient is in respiratory failure, intubation should be avoided at all costs. Intubating these patients can lead to a fatal hemodynamic collapse for two main reasons:

1.     Sedation -> Loss of native catecholamines -> decreased SVR/vasodilation -> decreased venous return -> cardiovascular collapse (1)

2.     Positive pressure ventilation -> increase RV and LV afterload and decreased RV preload -> decreased CO -> cardiovascular collapse (1)

Therefore try to avoid intubating these patients. If respiratory support is needed, first try NIPPV. This avoids the adverse effect of eliminating the patient’s innate catecholamine surge. In addition, the NIPPV can be removed rapidly if the patient begins to deteriorate. (1) If a patient needs to be intubated, following these guidelines can increase your chance of success.

1.     Place an arterial line prior to intubation in order to quickly assess any hemodynamic changes and respond appropriately.

2.     Avoid hypoxia -> preoxygenate the patient and utilize apneic oxygenation during the intubation

3.     Avoid hypercarbia -> induce respiratory alkalosis prior to intubation (4). Hypercarbia worsens pulmonary vasoconstriction.

4.     Consider performing awake intubation.

5.     Medications

a.     Induce with etomidate -> cardiovascular neutral (2)

b.     Paralyze the patient -> increases chances of first pass success

c.     Push dose pressors -> Have ready at the bedside along with your induction/paralytics (1)

d.     Have norepinephrine drip ready -> Have the pump primed and connected; just having the medication in the room is not good enough (1)

6.     Vent settings -> keep intrathoracic pressures low (similar to ARDS protocol) -> low TV, PEEP, low plateau pressures (2,3)

Further management

LVAD, ECMO, atrial septostomy, lung transplant, PH referral center (1,2,3)


1.     Pulmonary Hypertension and Right Ventricular Failure in Emergency Medicine, Wilcox

2.     Hoeper MM, Granton J. Intensive care unit management of patients with severe pulmonary hypertension and right heart failure. Am J Respir Crit Care Med. 2011;184:1114-1124

3.     Acute Right Ventricular Failure in the Setting of Acute Pulmonary Embolism or Chronic Pulmonary Hypertension: A Detailed Review of the Pathophysiology, Diagnosis, and Management

4.     Lahm T, McCaslin CA, Wozniak TC, et al. Medical and surgical treatment of acute right ventricular failure. J Am Coll Cardiol. 2010;56:1435-1446.

5.     Kwak YL, Lee CS, Park YH, et al. The effect of phenylephrine and norepinephrine in patients with chronic pulmonary hypertension. Anaesthesia. 2002;57:9-14

6.     Ternacle J, Gallet R, Mekontso-Dessap A et al. Diuretics in normotensive patients with acute pulmonary embolism and right ventricular dilatation. Circ J 2013;77:2612–2618.

7.     Schmid E, Hilberath JN, Blumenstock G, Shekar PS, Kling S, Shernan SK, Rosenberge P, Nowak-Machen M. Tricuspid annular plane systolic excursion (TAPSE) predicts poor outcome in patients undergoing acute pulmonary embolectomy. Heart, Lung and Vessels. 2015; 7(2): 151-158

8.     https://emcrit.org/podcasts/pulmonary-hypertension-right-ventricular-failure/

9.     https://www.nhlbi.nih.gov/health/health-topics/topics/pah/types

EKG of the Week 2017 4-2

This EKG comes courtesy of Dr. Adamakos.

An 88 y/o male presented to the ED after syncopal episode. Vital signs: Pulse 40, Respirations 14, BP 130/80. The EKG is below.

1.       What rhythm is demonstrated on this EKG?

2.       How would you manage this patient?



The rhythm is 3rd degree AV block (AKA complete AV block).

The patient is stable. Atropine can be attempted but is unlikely to be successful. Pacing pads should be placed on the chest. A cause of the heart block should be sought.


The EKG demonstrates a bradycardic rhythm at a rate of approximately 30. P waves are present but there are dropped P waves. The RR intervals are regular and the PR intervals are irregular. This is consistent with 3rd degree AV block.

Differentiating 2nd degree from 3rd degree AV block can sometimes be difficult. The following algorithm is useful.

If the patient is unstable, they should be treated with a transcutaneous pacer followed by a transvenous pacer. If the patient is stable, reversible causes should be sought. These include hyperkalemia, and toxicity from digoxin, beta blockers or calcium channel blockers. If no reversible cause is identified, the patient will need a permanent pacemaker.


EKG of the Week 2017 3-19

A 78 year old male with a history of CHF (EF 15%) and an ICD in place, presents to the ED complaining of palpitations and chest pain. His vital signs are: Pulse – 160, R 18, BP 140/80. He is awake and alert. His EKG is below.

1.       What is the rhythm demonstrated on the EKG?

2.       How would you manage this patient?



The rhythm is ventricular tachycardia

The patient is stable so he can be managed medically. However, this patient was managed with overdrive pacing. See below.


The rhythm is a wide complex tachycardia at a rate of ~160. In emergency medicine we always assume a wide complex tachycardia is V-tach. That is especially true in a patient with a history of CHF and especially true in a patient with an ICD. (Remember that an ICD is placed because the patient is at high risk for developing V-tach). This rhythm was confirmed to be V-tach.

If the patient was unstable, the treatment would be electrical cardioversion. Since the patient is stable, they can be treated with medications such as amiodarone. However, this patient was already on amiodarone. Other options include lidocaine or procainamide.

However, this patient has an ICD in place which presents other treatment options. In the words of a recent lecturer at the EMCrit conference, “Use the device”. We can use the device to shock the patient. Another option is using the device for overdrive pacing.

Overdrive pacing is a technique where a pacemaker is used to pace the heart at a rate faster than the tachyarrhythmia. Overdrive pacing provides a brief burst of paced beats. The idea is that if the pacemaker can take over, then when the burst is over the patient’s sinus beats can kick in and the tachyarrythmia is over. In fact, ICD’s often utilize the technique of overdrive pacing before they cardiovert the patient.

This technique was employed in our patient. The EP machine was used to control the pacemaker/ICD and a burst of paced beats was initiated. First a rate of 180 was attempted which was unsuccessful .The rate was then sequentially increased. A rate of 220 was ultimately successful in converting the rhythm to sinus. The rhythm strips of this are below.

The repeat EKG after overdrive pacing is below. The patient is now in sinus rhythm.

Overdrive pacing typically requires a transvenous pacer. Transcutaneous pacers have a maximum rate limit which prevents the use of overdrive pacing. There are case reports of transcutaneous pacers being used in the ED for overdrive pacing (Ann Emerg Med 1993 Apr;22(4):714-7; Ann Emerg Med. 1992 Feb;21(2):174-6.) but they require a special technique to achieve the appropriate rate.

Concussions: Tough Love

by Nicholas Otts, MD

edited by Gal Altberg, MD

A Common Problem:

16 y F presents with headaches, nausea, cloudy mentation, and irritability a day after heading a ball during a soccer game. You diagnose a concussion. Parents want to know when she should start exercising again and when she can go back to school?                          

 Two female soccer players competing for the ball, aerial view.

A Small Dose of EBM:

Many physicians commonly advocate for both physical and mental rest following concussion, but the evidence for that practice is lacking.  Let’s break it down into two areas, PHYSICAL and MENTAL.


Evidence for physical rest post concussion is based on old small observational studies, animal models, and “expert consensus” opinions, which in the EBM world is the same thing as letting the patient’s Mother and Google decide what is best.

Evidence that does exist suggests aerobic physical activity is beneficial in the initial week post concussion.

A prospective, multicenter cohort study showed physical activity within a week (versus no physical activity) was associated with reduced risk of persistent postconcussive symptoms a month later (1). A prospective randomized control trial showed similar benefit (2). Further, another study suggested that patients that had prolonged symptoms a week after the initial event, aerobic physical activity improved symptoms and was beneficial to recovery (3).

(*Important caveat: these studies refer to aerobic physical activity that does not risk further head injury. This does not mean the patient can return to whatever exercise activity he or she wants.)

Thus, the tough love advice of getting the athlete back on the exercise bike (but off the football field) is probably the better approach than nurturing them on the couch with Netflix and pizza.


The current approach is to suggest “mental rest,” until the patient has no further symptoms, which includes a prescription for staying home from school, avoid reading or writing, and “stimulating” video games.

The evidence for this approach is based on expert consensus and observational studies, which, again, is not ideal for clinical decision making (4,5,6).

1107_gsoccer1 01 1107_gsoccer1 01

A prospective trial previously mentioned (2) actually suggested that cognitive rest lengthened duration of post concussive symptoms.

Bottom line, if you prescribe cognitive rest or cognitive activity as tolerated, the evidence so far will not back you either way.  But I think it reasonable to suggest that children attempt as much mental activity as they can tolerate without worsening symptoms. Thus, the tough love approach in this scenario may also be best.


1 Grool AM, Aglipay M, Momoli F, et al. Association Between Early Participation in Physical Activity Following Acute Concussion and Persistent Postconcussive Symptoms in Children and Adolescents. JAMA 2016; 316:2504.

2 Thomas DG, Apps JN, Hoffmann RG, et. al. Benefits of strict rest after acute concussion: a randomized controlled trial. Pediatrics 2015; 135:213.

3 Leddy JJ, Kozlowski K, Donnelly JP, et al. A preliminary study of subsymptom threshold exercise training for refractory post-concussion syndrome. Clin J Sport Med 2010; 20:21.

4 Brown NJ, Mannix RC, O’Brien MJ, et. al. Effect of cognitive activity level on duration of post concussive symptoms. Pediatrics 2014; 133: e299.

5 Sady MD, Vaughan CG, Gioia GA. School and concussed youth: recommendations for concussion education and management. Phys Med Rehabil Clin N Am 2011; 22:701.

6 Howell D, Osternig L, Van Donkelaar P, et. al. Effects of concussion on attention and executive function in adolescents. Med Sci Spots Exerc 2013; 45: 1030.