Tag Archives: EKG

Conference Notes For 08/09/2023

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Infective Endocarditis Lightning Lecture

  • Pathophysiology: Usually starts with an insult to the endothelium, leading to formation of sterile vegetations. Then, an episode of transient bacteremia may seed an infection to these pre-existing vegetations
  • Infected vegetations often embolize, leading to a wide range of symptoms and secondary effects
  • Prevalence is as high as 10-15% in those who abuse IV drugs
  • The Modified Duke Criteria is used for diagnosis
  • When you suspect IE, three blood cultures from three different sights should be drawn
  • Antibiotic selection varies depending on native or prosthetic valve

Pericarditis and Myocarditis Lightning Lecture

  • Myocarditis is inflammation of the muscle cells of the heart. Can be acute, subacute or fulminant
  • Wide range of etiologies including viral/ bacterial infections and autoimmune diseases
  • Can lead to dilated cardiomyopathy and heart failure
  • Up to 80% of cases of pericarditis have an idiopathic etiology. Other causes include infections, radiation, Dressler’s syndrome
  • Pericarditis can lead to effusions/ adhesions, leading to constrictive pericarditis or even tamponade
  • Pericarditis does have some characteristic EKG findings. Important to differentiate from a STEMI

Pediatric Congenital Heart Disease

  • CHD is the most frequently occurring birth defect
  • Cyanotic lesions- think the “Five T’s” plus pulmonary atresia
  • When you’re concerned about a ductal-dependent lesion, don’t hesitate to give prostaglandins; biggest side effect is apnea, which can be managed
  • First two things to get when a newborn presents with suspicion of a CHD: All four extremity BPs and preductal+ postductal O2 sats
  • First two things to do during a suspected tet-spell: Squat/ knees to chest and give O2
  • If a baby is tachycardic, try to address potential secondary causes before giving adenosine

EKGs

  • When interpreting EKGs, especially early on you need to be systematic
  • A “significant” Q wave will be > 1/3rd the height of the R wave
  • When you see STD, you should be asking yourself “where is the STE?”
  • Most important factor to consider when evaluating for ischemia is the history, don’t get caught up too much on risk factors or lack thereof
  • Hyperacute T waves are broad-based, become asymmetric as the J point begins to elevate
  • Convex STE is very specific for ischemia
  • Don’t forget to get serial EKGs when there’s any suspicion; If you’re repeating troponin, you should also repeat EKGs. Don’t be afraid to get a quick repeat in 15-20 minutes when they’re actively in chest pain and you’re concerned

R3 Procedure Sim: Pericardiocentesis + Transvenous Pacing

  • Pericardiocentesis has three different approaches. No consensus on which is best
  • If performing the parasternal approach be careful to avoid the thoracic artery
  • Major indications for transvenous pacing include unstable bradycardia, sick sinus syndrome with pauses or failure to pace with the transcutaneous approach
  • RIJ is the preferred approach for floating a transvenous pacer

EKG in syncope

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Syncope is probably up there with dizziness for one of my least favorite ED complaints. Our job as emergency physicians however is to triage those who had simple vasovagal episodes from those who may have significant morbidity and mortality if we just let them go home. The purpose of this blog post is to list several important things I try to look for apart from the regular obvious EKG findings that would have us worried such as an acute STEMI, SVT, V-tach. Below are several other EKG diagnoses to keep an eye out for. See if you can dx the patient prior to the answer below. 

Case 1- 25 yo male with a history of palpitations presents after syncopal episode

EKG from Life In the Fast Lane

Diagnosis

  • Wolf-Parkinson-White syndrome

Pathophysiology

  • Presence of a congenital accessory pathway “Bundle of Kent” which predisposes a person to deadly arrythmias. 
  • Orthodromic
  • Antidromic 

EKG findings

  • Shortened PR interval < 120ms
  • Delta Wave: Slurred begning upstroke of the QRS complex
  • Wide QRS interval

 

Delta wave. Picture taken from wikiem.org

Management

  • If associated with atrioventricular reentry tachycardias we need to treat
  • Orthodromic conduction- Conduction from AV node back through accessory pathway
    • Narrow qrs
    • Stable Treatment- treat like SVT with Vagal maneuvers  adenosine, procainamide, calcium channel blockers 
    • Unstable treatment synchronized cardioversion
  • Antidromic conduction- conduction through the accessory pathway and retrograde via SA Node
    • Wide QRS
    • Stable treatment- procainamide, amiodarone consideration
    • Unstable treatment- Synchronized cardioversion

Disposition

  • Likely admission unless asymptomatic, known WPW, and cardiology can follow up very closely 

Case 2: 25 yo male with fever presents after syncopal episode

 EKG from Life in the Fast Lane

Diagnosis

  • Brugada Syndrome

Pathophysiology

  • Genetic sodium channelopathy with high risk for sudden cardiac death and Vfib arrest 
  • Dx requires ECG findings as well as:
    • Documented ventricular fibrillation
    • Family history of sudden cardiac death
    • Similar EKG in family members
    • Syncope

EKG findings

  • Right bundle branch pattern RSR’ in leads V1, V2
  • ST elevation in precordial leads V1-V3
  • ST elevations can have different morphology: >2mm in type 2 Brugada, > 1mm in type 3 Brugada

Management and Disposition 

  • If incidental- No acute treatment but will need very close follow up for pacemaker
  • If symptomatic- had syncopal episode and are now fine or active arrythmia admit with cardiology consultation for pacemaker

Case 3. 25 yo male with syncopal episode at soccer practice

Diagnosis

  • Hypertrophic obstructive cardiomyopathy aka HOCM

Pathophysiology

  • Genetic (1 in 500 individuals) condition which causes hypertrophy of cardiac muscles leading to possible left  ventricular outflow tract obstruction and syncope
  • Decreased compliance leads to poor filling and cardiac function
  • Symptoms worse with exertion typically

EKG findings

  • Left ventricular hypertrophy criteria S wave in V1 + R  wave in V5 > 35mm
  • “Dagger-like” Q waves can bee seen in anterolateral leads

Management

  • Avoid exertional activities
  • Needs ICD placement
  • Can have surgical myomectomy performed
  • Beta Blockers

Disposition

  • Cardiology consultation and admission for echo and ICD evaluation

Case 4 25 yo male with syncopal episode while watching tv recently started on azithromycin

EKG from wikiem.org

Diagnosis

            Long QT syndrome (LQTS)

Pathophysiology

  • Group of inherited conditions resulting in delayed ventricular repolarization

EKG findings

  • Corrected QT interval QTc of >450 in men and > 460 in women
  • QTc = QT /√R-R
  • Can guestimate about half of the R-R interval as well

Management

  • Unstable- defibrillation
  • Stable
    • Stop any QT prolonging medication
    • Magnesium sulfate IV
    • Consider amiodarone

Disposition

  • If symptomatic or QT > 500 consider admission

Case 5. 25 yo male presents s/p sudden cardiac arrest with ROSC after defibrillation 

EKG from Life in the Fast Lane

Diagnosis

  • Arrhythmogenic Right Ventricular dysplasia

Pathophysiology

  • Inherited myocardial disease where you get fibrofatty infiltration and thinning of the RV myocardium, RV dilation, global systolic dysfunction

EKG findings

  • Epsilon wave – small positive deflection at the end of the qrs (most specific finding, seen in 30% of patients) 
  • Can be confused for Osborn J wave
  • Prolonged S wave Upstroke (95% of patients) similar to WPW

Management

  • Treat arrythmias 
  • Sotalol and Amiodarone
  • Urgent ICD placement

Disposition

  • Admission if symptomatic
  • Very close follow up if incidental finding

Summary: 

In every EKG one should take a quick glance at the wave morphology to look for signs of WPW, HOCM, ARVD, LQTS, and Brugada ( I know that’s a lot of abbreviations). I can’t say that I have found any of these yet in my syncope patients but as Dr. Thomas told me if you never look for them you will never find them. 

Extra: I found a great pictoral from ALIEM for can’t miss EKG findings that has the changes listed above and more. I have listed it below for your reference. 

Sources: Life in the Fast Lane , Wikiem.org, ALIEM

Prolonged QT

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58 yo F presents to the ED for cough, chest pain, and fatigue for 1wk. She has sharp, atypical sounding chest pain. But she is 58 and has risk factors: HTN, HLD, 0.5ppd smoker x48yrs. Better get an EKG.

Prolonged QT EKG

Initial EKG

Awesome, no STEMI. Done with EKG right? Hope you didn’t miss that really long QT interval.

First, how do we measure the QT?

QTc imageWe usually talk about QTc rather than just the QT. This is because the QT interval varies depending on the HR. Using a correction equation standardizes the interval so it can be interpreted regardless of the HR. The EKG computer does give a calculation of the QTc, because we are obviously not hand calculating this on every patient. You should compare what the computer calculates to your gestalt when you review the EKG. If there are any concerns or discrepancies, you should hand calculate the QTc. MDCalc has an easy to use calculator. Above is the Bazett’s formula, which seems to be the most commonly used. Other formulas do exist. QTc is considered prolonged if > 440ms in men or > 460ms in women.

Next, why do we care?

ecg_hypokalaemia_torsades

This is the start of Polymorphic VT. There are several things that can cause this rhythm. Long QT is one possible cause. When Polymorphic VT is caused by a prolonged QT we give it a special name, torsades de pointes. The mechanism behind this is demonstrated on the above EKG. As the QT interval becomes more prolonged, there is a higher chance for an R-wave to hit on just the right part of the T-wave and cause this rhythm. QTc > 500ms seems be associated with higher risk.

So what causes prolonged QT?

Many things can cause prolonged QT. The most common etiologies are electrolyte abnormalities and drugs. Hypokalemia, hypomagnesemia, and hypocalcemia are well known to cause prolonged QT. Potassium and calcium are included on the CMP but don’t forget about magnesium. Drugs are also a big cause of prolonged QT. The list of drugs is long. Probably too long to memorize. However, there are some common medications and medication classes that you should know. The big classes are, Antiarrhythmics (like Amiodarone), Antihistimines (like Diphenhydramine), Macrolides (like Erythromycin), Antipsychotics (like Haloperidol), and TCAs (like Amitriptyline). This is not a complete list, just some highlights. If you really want to know if a specific medication is associated with prolonged QT, www.crediblemeds.org is a good source.

Other causes worth mentioning are structural heart disease, cardiac ischemia, and stroke. Some people do have Congenital Long QT Syndrome, but this should not be the leading diagnosis in the ED. Also those people are still at high risk for developing Polymorphic VT.

How did our patient do?

Her medications were reviewed and she was not on any of the most common offenders. Then routine labs came back. Unremarkable, except for K of 2.9! Repeat EKG after potassium repletion.

Normal EKG

EKG after K repletion

 

References:

  • www.uptodate.com
  • http://lifeinthefastlane.com/ecg-library/basics/qt_interval/
  • http://hqmeded-ecg.blogspot.com/2013/10/polymorphic-ventricular-tachycardia.html
  • bjsm.bmj.com/content/43/9/657/F3.large.jpgamp

Reasons not to get into prison fights…

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Middle aged male transferred from an OSH, accepted by ENT for a mandible fracture.

The patient is incarcerated, and was involved in an “altercation” with other inmates. The incident occurred around 2PM; but he didn’t report any of his pain to the guards until 10PM.  On arrival at the OSH he had multiple contusions to his face/head, lacerations over his hands, and obvious dental trauma.  The patient was also complaining of chest pain – he stated that another inmate had slammed him in the chest with his knee. Despite his age, the patient has a history of previous MI in 2011, cathed at U of L with no stents placed. Takes a baby aspirin, no other meds and no other PMH.

At this point, the patient is about 10 hours out from the incident. Work-up at the OSH with the following: neg CT head and CXR. CT face with a mandible fracture. Labs notable for WBC 17.8, Hgb 14.3, platelet 373, normal coags, normal electrolytes, BUN/Cr 14.0/1.1. Total CK 213 (55-170 normal), troponin <0.012, CKMB  1.66 (0 – 3.38 normal), myoglobin 271.8 (0-121 normal).  Tox screen negative. EKG is as follows:

OSH EKG

His hand lacerations were repaired and he was started on Augmentin for a human bite. ENT accepted, and the patient was transferred to U of L, arriving about 6 AM. Dental was consulted on arrival and splinted his teeth. By 9 AM ENT had evaluated the patient and admitted him to the floor, planning for surgical intervention.

The patient was an ED floor hold, and around 2PM began complaining of worsening chest pain. ENT was paged and ordered an EKG and a set of cardiac enzymes, coming down to re-eval the patient. His EKG now looked like this:

1410 EKG

Enzymes came back with CK total 5024, CKMB 303, and troponin 44.1. Cardiology was consulted and ordered a stat echo and started the patient on ACS protocol. The echo showed an EF of 30%, an akinetic mid/distal anferoseptum and an akinetic apex. Cards initially thought that this was consistent with stress cardiomyopathy in the setting of trauma, but couldn’t rule out cardiac ischemia due to direct cardiac trauma. They planned to treat medically and cath in the morning.

Throughout the evening, he developed worsening ST elevation in his lateral leads and his troponin continued to rise, up to 67.0 by midnight.

0308 EKG

The on call cath attending at Jewish was consulted and by about 3AM the decision was made to transfer the patient to Jewish for a cath first thing in the morning.

Final result: 100% LAD occlusion, secondary to direct cardiac trauma.

Definitely rare injury, but one to keep in the back of your mind, especially as it can occur in previously healthy, relatively young patients. Of note, these can have delayed presentations, up to several days. Typically occur after MVA, but there are several cases reports occurring after crush injuries, being hit in the chest by a soccer/rugby ball, and my personal favorite, one listed as “struck in the chest by an umbrella tip.”