EKG Case Study: Is There More to This Chest Pain?

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Author: Ashley Grigsby, DO, PGY-4
Combined Emergency Medicine/Pediatrics
Indiana University

Case
A 32-year-old previously healthy African American male presents via emergency medical services (EMS) for evaluation of chest pain. An ST elevation myocardial infarction (STEMI) code had been activated by EMS based on pre-hospital electrocardiogram (EKG) that had been interpreted as ST elevation in the anterior leads with reciprocal ST depression in the lateral leads. On arrival to the emergency department (ED), the patient appears ill and reports severe crushing chest pain radiating to the arm and down into the abdomen. He is diaphoretic and clutching his chest. His heart rate is 123 beats per minutes, respiratory rate 16 breaths per minute, and blood pressure 210/110 mmHg. He is afebrile. Initial ED EKG is shown below.

Board Review: Making Decisions Based on the EKG

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Image Credit: US Air Force

Author: Nick Pettit, DO PhD, PGY-2
Indiana University
AAEM/RSA Social Media Committee

Case
The setting is a busy shift in your high-acuity pod of your emergency department. You just walked out of room 1 after resuscitating a tricyclic antidepressant (TCA) overdose. Then overhead you hear, “trauma 1 here, room 4,” and at the same time your nurse hands you the below electrocardiogram (EKG).

As you are walking toward room 4 and scribble “non-ST-elevation myocardial infarction (non-STEMI),” she gives a quick history about this patient. The patient is a 77-year-old male with a past medical history of some kidney and heart issues, and he now has fatigue, shortness of breath, and bilateral lower extremity edema. Just as you pop into the trauma in room 4, you tell your nurse you will be right over, but to please draw a rainbow of labs and:

1. Administer 40 mL/kg 0.9% NaCl bolus.
2. Administer 3 g calcium gluconate.
3. Administer 6 vials of digi-bind.
4. Administer 40 mEQ of potassium chloride
5. Place pads and pull up ketamine for procedural sedation and immediate cardioversion.
6. Call poison control.

Correct answer
B. Administer 3 g calcium gluconate. This patient has hyperkalemia, and based on the EKG, it should not be surprising if their potassium returns at greater than 9.0.

This review will focus on the causes of hyperkalemia, its identification, and its immediate treatment.

Causes

1. Decreased excretion, such as in renal failure (as in this case)
2. Excessive potassium intake
3. Increased production of potassium (rhabdomyolysis, tumor lysis, trauma)
4. Redistribution (digoxin, acidosis)[1]

Identification

1. Basic metabolic panel (BMP). Be sure to watch for hemolysis, which can cause pseudohyperkalemia.
2. EKG. Different levels of potassium elevation can cause unique EKG findings:[2]
• ~6.0 = peaked T waves
• ~7.0 = P-wave evolution
• ~8.0 = wide QRS
• ~9.0 = sinusoidal appearance

Symptoms
Weakness, confusion, chest pain, nausea and vomiting, palpitations

Management

1. Calcium
• Calcium chloride if there is a central venous catheter (CVC), or calcium gluconate if there is peripheral access only.
• Stabilizes membrane in approximately ten minutes, with EKG returning to normal over several minutes.
2. Insulin and glucose
• Ten units of insulin given with dextrose.
• Works over 30 minutes
3. Sodium bicarbonate
• Helps correct acidosis
4. Albuterol
• Shown to lower potassium 1 mmol/L in healthy subjects
5. Dialysis
• May need emergent dialysis. Remember the AEIOU mnemonic:
• Acidosis
• Electrolyte disturbances
• Ingestion
• Overload (fluid)
• Uremia
• In the above case, the patient may benefit from emergent dialysis.
6. Furosemide
• May help if the patient is volume-overloaded, but this is a common disease in end stage renal patients and furosemide may have limited value here.[3]

References:

1. Rodriguez, J., Calvert J. Hyperkalemia. Am Fam Physician. 2006 73(2):283-290

2. Hall, B., Salazar, M., Larison, D. The sequening of medication administration in the management of hyperkalemia. J of Em Nurs. 2009 35:4;339-342

3. Wrenn, K., Slovis, C., Slovis B. The ability of physicians to predict hyperkalemia from the ECG. Annals of Emerg Med. 1992 20:11;1229-1232

Image of the Month (From August/September 2013 Modern Resident)

Author: Michael Gottlieb, MD
Cook County Emergency Medicine Residency
Originally Published: Modern Resident August/September 2013

An 81-year-old man with PMHx of HTN, DM, HL and OA s/p right hip replacement presents to the ED with acute onset CP and SOB x 1 day. While watching TV earlier, he developed a sudden inability to catch his breath, as well as some poorly localized, pleuritic chest tightness on the right side of his chest. He initially attributed this to reflux, but when it did not improve he drove himself to the ED.

His initial vitals are: Temp: 98.2, HR: 56, BP: 132/78, RR: 28, O2 Sat: 89%. Upon examination, he is in moderate distress, appreciably tachypneic and has to stop halfway through his sentences to catch his breath. The remainder of his exam is significant only 2+ pitting edema bilaterally. Labs are pending, a chest X-ray is ordered and his ECG is shown below.

Photo of the Month (From Apr/May 2013 Issue of Modern Resident)

Author: ENS Dylan Hendy, MSIV
Arizona College of Osteopathic Medicine
Author: LT Christopher D. Helman, DO
Naval Medical Center Portsmouth
Originally Published: Modern Resident, April/May 2013

Patient Vignette
Twenty-nine-year-old male was sent to the ED by a community clinic for a syncopal episode. The patient originally visited the clinic for a headache that resulted from a shelf falling on the back of his head while working in his garage two days earlier. The patient denies losing consciousness, amnesia, disorientation or N/V. However, upon further questioning the patient described an unwitnessed episode of “blacking out” while sitting in his car today. He states this episode may have lasted for 30-60 minutes. The clinic subsequently sent the patient to the ED for further workup. In the ED the patient explained that he has a history of chronic headaches and that his headache at present is similar with regards to onset, location and duration. However, to the best of his knowledge, today’s unwitnessed syncopal episode was a first time occurrence. Further ROS were negative. The patient has no other pertinent PMH and is taking no medications. Complete physical exam was unremarkable. A workup for a closed head injury and syncopal episode was performed. Laboratory data was WNL. Non-contrast CT head and CXR were both unremarkable. The following ECG was obtained:

Image Credit: Modern Resident

A Cannot Miss Cause of Bradycardia

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Author: Daniel Balk, MD
Emergency Medicine Resident
Drexel University College of Medicine

The Case:

The tech hands the physician this EKG:

It’s slow with a rate of 37, it’s irregular, it’s wide with a QRS of 130, it’s scary, and there is no previous EKG. The tech doesn’t know the patient’s story as “he speaks only Portuguese” and his chief complaint is hypoglycemia.

Glancing at the monitor as the physician rushes towards the room, the blood pressure is 138/71. This elderly Brazilian traveller (with a prior history of two cardiac stents, hypertension and diabetes) is discussing with his family whether his two days of diarrhea caused his sugar to be low all day despite foregoing his insulin. His blood glucose was 40 this morning; it’s 135 now after eating normally all day and skipping his long acting and mealtime insulin doses. The review of systems is entirely negative other than for diarrhea and hypoglycemia. Other than marked bradycardia, the exam is unremarkable.

Cardiac Infarctions Under Disguise

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Author: Joshua Bowers, DO 

Emergency Medicine Resident
Adena Regional Medical Center

Ischemic heart disease and coronary artery disease (CAD) are two of the leading causes of death among adults in developed countries.[6] Patients with these disorders can present to the emergency department with problems that fall anywhere along the spectrum of clinical diseases referred to as acute coronary syndrome (ACS). ACS is the result of myocardial ischemia and can range from unstable angina to ST-segment elevation myocardial infarction (STEMI) that requires emergent intervention. STEMI requires immediate recognition; however not all STEMIs present with elevations on the initial standard 12-lead electrocardiogram (ECG).[1]

In general, ECGs provide a rapid way to evaluate for signs of cardiac ischemia and rhythm disturbances. While the ECG is one of the best tests in the emergency department to assess and evaluate the evolution of ACS, ECGs have limitations. One of these limitations is the inability to evaluate the posterior wall.[3,6]

EKG Rounds: Trauma Induced EKG Changes

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Author: Meaghan Mercer, DO
Emergency Medicine Resident
University of Nevada School of Medicine
AAEM Resident and Student Association President

A 35 year old male presents to the ED after a motor vehicle collision with ejection. The patient has a Glasgow Coma Scale of 4 on arrival and is immediately intubated. The patient has equal pupils and has facial and chest abrasions. The patient is initially tachycardic with a heart rate of 115. He is normotensive and saturating well on the ventilator. A bedside ultrasound shows no pneumothorax and FAST examination is negative. While waiting for the patient to go to CT an EKG is obtained.

What does the ECG show?

Brugada-type EKG inducers

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Author: Kristin E. Fontes, MD
Academic Fellow/Clinical Instructor, Division of Emergency Medicine
Stanford University

Case
A 6 year old boy is sent to the ED by his outpatient cardiologist for fever. He has a history of an abnormal pattern on EKG when he has a fever. He has an implantable loop recorder. Below is a portion of his EKG obtained on arrival to the ED. His temperature was 101.2. What is the diagnosis?

The patient’s EKG shows a Brugada pattern. Here (cited below) is a small study that looked at 47 patients who presented with Brugada-type EKGs and identified potential inducers. Some patients had the common SCN5A mutation, while some did not. Patients may be asymptomatic or have syncope/sudden cardiac death whether or not they have the mutation.

Reported Brugada-type EKG inducers

• Fever
• Drugs with sodium channel blockade properties (cocaine, TCAs, antidysrrhythmics, anesthetics) 
• Propofol

Management priorities in the emergency department
The most important aspects of treatment are stabilization of malignant arrhythmias as well as fever control and/or removal of the offending agent, if applicable. Cardiology consultation is warranted for consideration of genetic testing, electrophysiologic studies, and potential ICD placement.


References

Junttila MJ, Gonzalez M, Lizotte E, et al. Induced Brugada-type electrocardiogram, a sign for imminent malignant arrhythmias. Circulation. 2008;117(14):1890-3.

Allely, Peter. What is Brugada Syndrome?. Life in the Fastlane Blog, http://lifeinthefastlane.com. http://lifeinthefastlane.com/what-is-brugada-syndrome/. Accessed January 12, 2015.

Updates on LBBB and STEMI

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Author: Meaghan Mercer, DO
Emergency Medicine Resident
University of Nevada School of Medicine
AAEM/RSA President

I recently attended the #Resus14 conference in Las Vegas and Dr. Amal Mattu asked the audience how many felt comfortable with the Sgarbossa criteria. I was surprised at how few hands went up. Repetition is the key, but if you think you had Sgarbossa down there are some changes!

New LBBB is no longer a STEMI equivalent *UNLESS*
a. The patient has new heart failure

b. The patient is unstable
c. The EKG meets Sgarbossa A or B criteria

Increasing the Paper Speed in Narrow-Complex Tachycardia

Normal paper speed (25mm/s)

Authors: Destinee DeLemos, MD
Nathan Haas, MD
University of Michigan Department of Emergency Medicine





Narrow complex tachycardia often presents a diagnostic and therapeutic dilemma, and one simple trick can help in the correct identification of the underlying rhythm. With increasing heart rates, it becomes quite challenging for the emergency physician to distinguish between sinus tachycardia, paroxysmal supraventricular tachycardia (pSVT), atrial fibrillation and atrial flutter. If the underlying rhythm is not pSVT, an unnecessary adenosine trial can prove quite unpleasant for both the patient and physician.

Increased paper speed (50mm/s)
Images Courtesy of Amal Mattu, MD FAAEM

Standard 12-lead EKGs are printed at 25mm/second. By simply doubling the paper speed to 50mm/second, the printed rhythm strip appears widened and exaggerated, which can aid in identifying finer details of the EKG. The images in this post demonstrate previously hidden flutter waves becoming more apparent at an increased paper speed.

Cardiology Pearl: Wellens' Syndrome

Photo: Wikimedia Commons
Click to Enlarge

Originally Published: Modern Resident, Aug/Sep 2011

Original Author: Alan Sielaff, MS IV Loyola University Chicago, Stritch School of Medicine

Submitted by: Rachel Engle, DO Communications Committee Co-Chair
 
A 63 year old female with a history of hepatitis C and diabetes mellitus presents to the emergency department after experiencing acute substernal chest pain, SOB and emesis during a routine visit to her PCP earlier this afternoon. All symptoms spontaneously resolved shortly prior to her arrival in the ED. She has no other complaints and a normal physical exam. Her EKG is shown above.