A 56 year old female with a history of asthma, hypothyroidism, tobacco use, chronic opioid use was found down at home,  found to have subarachnoid hemorrhage, left temporal hematoma with bilateral supraclinoid aneurysms on CTA, s/p embolization. Hospitalization has been complicated by vasospasm, fevers, long QT, and stress induced cardiomyopathy. On hospital day 11 the following EKG was obtained to assess the patient's long QT noted on previous EKGs (500, 516, 620).  

Rate 89, sinus rhythm with sinus p waves, left axis deviation, normal PR, QRS  intervals, prolonged QTc 732. T-wave inversions in I, II, III, aVF, V2-V6. In fact, if you pay attention to the T-wave morphology you will notice polymorphic deep t-waves, alternating in depth and morphology. There are two interesting points from this EKG: 1) T-QT pattern, and 2) T wave alternans. 

T-QT pattern: 

• Large, sometimes global T wave inversions
• T waves may be giant negative; occasionally giant positive
• Prolonged QT
• This is a stereotypical response to a variety of noxious stimuli, most notably acute CNS disorders, catecholamine effect, emotional stress (Tako-Tsubo cardiomyopathy), pulmonary edema, and massive PE. 
• This patient has both acute SAH, as well as catecholamine effect (recent adrenergic stress and pressors). 
• Usually evolves ~24h after the insult. Dr. Littman refers to this as the "day after" EKG. 

T wave alternans: 

• Beat to beat variability in the timing OR morphology of repolarization.
• Indicative of depolarization heterogeneity, which increases susceptibility to ventricular tachyarrythmias. 

Approximately 2 hours after the above EKG, the following rhythm strip was noted on telemetry. 
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Here you see a PVC followed by a compensatory pause, followed by polymorphic VT.  Pauses are frequent triggers of Torsades. The patient went on to experience several sustained, and non-sustained runs of polymorphic VT overnight. She received aggressive Mg & K repletion, defibrillator pads were placed, but patient remained hemodynamically stable and did not require defibrillation or overdrive pacing.  QT decreased and VT resolved. 

Teaching points:

• Acquired long QT is mostly iatrogenic, however not in this case. Other important causes of acquired long QT include acute CNS abnormalities, and acute stress cardiomyopathy. 
• Many medications can prolong QT, notably most psych medications, and antibiotics including quinines, macrocodes, azole antifungals. Electrolyte abnormalities are also often a culprit. 
• T wave alternans is a harbinger of ventricular tachyarrythmias. 
• Patient with prolonged QT need close telemetry monitoring, as well as aggressive K & Mg repletion to the upper limits of normal (K>4, Mg>2). 
• If patient experiences give 2mg MgSO4 IV, can repeat x 1. 
• If Torsades persists after Mg x 2, consider low dose isoproterenol or increasing heart rate by overdrive pacing, or giving a chronotrope such as dobutamine while you pursue emergent cardiology consultation. 
• Overdrive pacing should be transvenous, as opposed to transcutaneous, as there is not 1:1 capture with transcutaneous pacing, and pauses can trigger further episodes of tachyarrythmia. 

References: 
Warraich H, Buxton A, Kociol R. Macroscopic T-wave alternans in a patient with takotsubo cardiomyopathy and QT prolongations. Heart Rhythm. 2014 Oct;11(10):1848-9.
 
Sommargren C, Drew B. Preventing torsades de pointes by careful cardiac monitoring in hospital settings. AACN Adv Crit Care. 2007 Jul-Sep;18(3):285-93

Clinical context: This is a 20s year-old male who presented to the ED after GSW to the thorax. He lost pulses in transport, and underwent ED thoracotomy, cardiac massage and aortic cross clamping with ROSC, and subsequent ex-lap. He has been in the ICU with complications including respiratory failure, renal failure, hemorrhagic shock, and multiple returns to the operating room for intrabdominal injuries. The following EKG was obtained over the weekend due to ST elevation noted on cardiac telemetry.  

Automated read notes sinus tachycardia, ****ACUTE MI/STEMI****

Let's systematically review this ECG. The ventricular rate is 126, there is a p wave before every QRS - sinus rhythm, QRS is upgoing in I, II - normal axis, PR, QRS intervals appropriate, QTC prolonged at 492, there is ST elevation in I, II, III, aVF, V2-V6 with concomitant PR depressions, reciprocal ST depressions and PR elevations in aVR and V1.  

This is a classic ECG for PERICARDITIS. 

The patient subsequently had cardiac ultrasound that demonstrated a small effusion as well. 

Remember that classic findings of pericarditis include widespread ST elevation and PR depression with reciprocal changes in aVR +/- V1. 

Life in the fast lane review of pericarditis 

While there are many causes of pericarditis, this patient has several underlying risk factors including chest trauma, surgery, and possible infection secondary to limited sterility in the emergency setting. While the reported incidence of acute pericarditis after general thoracic surgery is very low, I was not able to identify any recent literature addressing the incidence of pericarditis after ED thoracotomy in patients without penetrating cardiac injuries. In patients with penetrating cardiac injury delayed secondary cardiac injuries and complications occur at at rate of ~50%. Colchicine is noted to be used as pericarditis prophylaxis in major cardiac surgery and transplant, this could be considered in the ED setting, however the logistics and lack of evidence as to how common this complication is could limit benefit. 

Complications of ED Thoracotomy include:

• Neurologic complications from hypoperfusion: Anoxic brain death occurs in as many as 50% of survivors, requiring ongoing institutional care. 
• Recurrent bleeding from chest wall or internal mammary artery
• Damage to the coronary arteries
• Other cardiac damage resulting in ventricular septal defects, aortic valvular irregularities, atrial septal defects, and cardiac conduction defects
• Damage to the esophagus during aortic cross-clamping
• Damage to the phrenic nerve
• Ischemia to distal organs and spinal cord due to cross-clamping of aorta

http://emedicine.medscape.com/article/82584-overview#a9

Upon return to the OR the day after thoracotomy this patient was noted to have ongoing bleeding from internal mammary arteries, but no damage to coronary arteries or other cardiac damage.  
 
References:
Imazio, M., Gaita, F., LeWinter, M. Evaluation and Treatment of Pericarditis A Systematic Review. JAMA. 2015;314(14):1498-1506.
Fallahnejad M., Kutty AC., Wallace HW. Secondary lesion of penetrating cardiac injuries: a frequent complication. Ann Surg. 1980;191(2):228.
Alraies MC, AL Jaroudi W, Shabrang C, et al. Clinical features associated with adverse events in patients with post-pericardiotomy syndrome following cardiac surgery. Am J Cardiol. 2014 Nov;114(9): 142630.
Keller D, Kulp H, Maher Z, et al. Life after near death: Long term outcomes of Emergency department thoracotomy survivors. J Trauma Acue Care Surg. 2013 May;74(5):1315-20.
 
 



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HPI: A previously healthy, incarcerated, 43 year old Asian American male presented to the ED after a syncopal episode with subsequent VF arrest. The patient is successfully defibrillated. After ROSC the following EKG is obtained: 

Normal rate, regular rhythm, sinus P waves in from of QRS. normal PR, normal QRS width, axis, amplitude, progression.  ST elevation in V1, V2, inverted T waves in V2, normal QTc.

After obtaining this EKG the patient was rushed to the cath lab, no obstructive coronary lesions were identified. 

What is the diagnosis, and what is the treatment? Is this finding always pathological? 

The diagnosis is Brugada syndrome. 

​ - syndrome is a constellation of Brugada pattern EKG + CLINICAL SYMPTOMS 

Brugada Pattern EKG: 
-RBBB pattern in V1  (rSR', terminal positive QRS complex)
-high take off, upward convex, ST elevation in V1 and V2
-inverted T waves in V1 and V2 

Clinical Symptoms:  syncope, +/- palpitations,  unexplained VF/arrest, family history of sudden death. 

Brugada Syndrome: 
-due to poorly understood sodium chanellopathy. There is NO UNDERLYING STRUCTURAL HEART DISEASE. 
-except for V1-V2, the EKG is usually normal. 
-Brugada pattern on EKG can be transient, and can be unmasked by physical stressors, medications, metabolic derangements, and ischemia. 

Treatment: ICD is indicated for patients with Brugada syndrome.

Brugada Pattern EKG is NOT ALWAYS pathalogical.
-Brugada pattern EKG can be a normal variant, especially in a patient without risk factors, symptoms, and the pattern is an incidental finding during a non-cardiac workup. 
-Brugada pattern can also be seen in severe hyperkalemia, sodium-channel blocker toxicity, propofol infusion syndrome, right ventricular pathology or injury. 

Patients who are incidentally found to have Brugada pattern EKG without cardiac symptoms are at low risk for sudden cardiac death. These patients should be educated on finding, referred to cardiologist, and given careful follow up precautions if they develop syncope, palpitations, chest pain, or other cardiac symptoms. A careful family history to elucidate family members with sudden cardiac death is warranted. There is some risk if the patient has Brugada EKG pattern without symptoms, but does have a family member who experienced sudden cardiac death. These patients should be referred to a cardiologist, and may undergo provocative testing to induce VT/VF, although this is controversial. 

References: 
1. Littmann, L. Monroe, MH., Kerns, WP., Svenson, RH., Gallagher, JJ. Brugada syndrome and "Brugada sign": clinical spectrum with a guide for the clinician. Am Heart J. 2003 May;145(5):768-78.
2. http://lifeinthefastlane.com/ecg-library/brugada-syndrome/