EKG of the Week – Week 27
In honor of the inservice coming up, here are a bunch (like way more than I intended when I started this email) of quick hits from the cards section. Basically think of it as important EKG findings (except ACS, which is a whole other huge topic) for the inservice! Disclaimer, these are things I think are important, but are no means an exhaustive list of all the important cards thing. Most of this is from First Aid and Life In The Fast Lane.
First off, what is sinus rhythm?-Rate of 60 – 100-p wave before each QRS with a 1:1 ratio-Upright p in II
Normal intervals?-PR interval 0.12 – 0.20 seconds- QRS <0.12 msecQT interval? I remember 450, women can be up to 460 and men can be up to 440
Ok, enough normal, talk about abnormal:
Let’s start with Blocks!
First Deg AV block: simple. PR interval >20 msec. that’s it. needs no treatment. Move on. Wanna see examples? https://lifeinthefastlane.com/ecg-library/basics/first-degree-heart-block/
Second Deg AV Block:
-Type 1) Wenchebach – PR interval gets longer and longer until a QRS complex gets dropped. Often unexciting and rarely needs a pacemaker or treatment. Like 1st Deg, can be seen with healthy hearts. https://lifeinthefastlane.com/ecg-library/basics/wenckebach/
****Can be seen if patient is having an INFERIOR MI****
-Type 2) QRS complexes are RANDOMLY Dropped, DOES NOT OCCUR IN HEALTHY HEARTS Associated with damage to the conducting system BELOW the AV node (infranodal) Assoc with ANTERIOSEPTAL MI Can Degenerate into 3rd degree without warning, ADMIT for pacer https://lifeinthefastlane.com/ecg-library/basics/mobitz-2/
Third Degree AV Block: NO Association between the ventricles and the atria. Think of this when the patent has an ANTERIOR / ANTERIOSEPTAL MI. Often the rate will be <40.
Some tips from first aid to determine if it is a nodal block or infranodal block: Nodal blocks show JUNCTIONAL Escape rhythms. They will be NARROW and the rate is 40-60 Infranodal blocks show VENTRICULAR Escape. They will be WIDE and rate <40 Why is this important? Because you can have a 3rd degree blocked rhythm that is NARROW. Be careful.Why does this matter? If you give atropine to a patient with an INFRANODAL block, it can WORSEN the conduction rate
https://lifeinthefastlane.com/ecg-library/basics/complete-heart-block/
Enough Blocks, How about extra beats?
PACs vs PVCs: Both are often totally normal. However, to tell the difference, PACs show a NONCOMPENSATORY Pause (this means that the next sinus beat comes EARLIER Than expected) where as PVCs show a COMPENSATORY Pause (The next beat occurs at an expected interval)
3 PVCs in a row = Nonsustained VTach
PAC: https://lifeinthefastlane.com/ecg-library/premature-atrial-complex-pac/
PCV: https://lifeinthefastlane.com/ecg-library/basics/pvc/
Ok, big stuff now, DYSRHYTHMIAS:
Couple big categories: Fast vs Slow and Narrow vs Wide and Regular vs Irregular. Let’s start with Slow!
Slow: Not a ton to say here. Vent rate <60. Try atropine, you can always pace them. Sick Sinus Syndrome EKG looks like an irregular rhythm with pauses in sinus activity, can degrade into a sinus arrest. That’s about it… Now onto Fast!
Fast:
Break it down:
Narrow and Regular: Sinus Tachycardia, Atrial Tachycardia, Atrial Flutter with a fixed block (remember if you see a rate of 150 on the exam LOOK FOR FLUTTER WAVES), and AVNRT (colloquially called SVT)
Narrow and IRREGULAR: Sinus tach with PACs (remember that non compensatory pause?), Afib, MAT, Atrial flutter with variable block
Wide and Regular: Regular SVT with BBB, Regular SVT with preexcitation, Vtach, V Paced (Check every EKG for pacer spikes)
Wide and IRREGULAR: Irregular SVT with BBB, Irreg SVT with preexcitation, VFib, Torsade de pointes
When I get an EKG on the test and it’s fast, I ask myself, is it wide or narrow and is it regular or irregular. Once I figure those two things out, it makes it easier to pick the right answer. You guys know what to do from here. SVT gets Adenosine, Afib with RVR or Aflutter gets Dilt, MAT treat the underlying cause, Defibrillate VFib, Cardiover VTach with a pulse, Defib VTach without a pulse, etc.
DO NOT Defibrillate someone with a pulse. You lose so many style points
Synchronized cardiovert someone with an unstable rhythm such as Afib with RVR or SVT (i.e. if the patient is hypotensive and in fib with RVR, do not give them dilt)
Big things to know for the test: Read the stem before looking at the EKG. You may get a patient with a poor quality EKG but he’s a smoker with COPD and it’s a narrow irregular rhythm. Boom. MAT.
Speaking of AFib, just glance at the CHA2DS2-Vasc (https://www.mdcalc.com/cha2ds2-vasc-score-atrial-fibrillation-stroke-risk) Hopefully it won’t come up but big take aways are that if you have a score of 1, you get a full dose aspirin every day. Anything over that you get anti-coagulated. I feel like a had 2-3 rosh questions on it and I was sad about that.
Couple of big hitters for the WIDE COMPLEX TACHYCARDIAS:
VTach: Monomorphic VTach is the most common form (i.e. the beats all look the same). The rate is roughly 150-200. You can see capture and fusion beats in VTach (https://lifeinthefastlane.com/ecg-library/ventricular-tachycardia/)
What to do for VTach:
1) No pulse? Defib
2) Pulse but unstable: Synchronized cardiovert
3) Pulse and stable: first line drugs are Procainamide or Amiodarone; Second line drug is lidocaine. If they don’t work, shock em.
Polymorphic Vtach: Two main testable categories here:
1) Torsades: usually due to PROLONGED QT (likely 2/2 drugs). Give IV Mag (1-2g over a minute then 1-2 / hr). If that doesn’t work, consider overdrive pacing. AVOID procainamide
2) Bidirectional VT: Axis changes by 180 degrees beat to beat. Crazy cool to see. SEVERE DIGITALIS TOXICITY. Give Digifab. https://lifeinthefastlane.com/ecg-library/basics/bvt/
VFib: Totally disorganized ventricular depolarization. Not good. Defibrillate. https://lifeinthefastlane.com/ecg-library/ventricular-fibrillation/
Ok, Enough of that.
Let’s Talk syncope. You have a 20 year old basic trainee who presents after falling out of PT. What do you look for on his EKG?
My Mneumonic: I get my HEB @ DQ:
H: HOCM Young person with EXERTIONAL SYNCOPE. You will see dagger (deep and narrow) Q Waves in the LATERAL AND INFERIOR LEADS. The murmur gets WORSE with valsalva (because valsalva decreases LV filling) Admit for an Echo. It’s ok to treat with Beta blockers or CCB, AVOID nitrates and ionotropes. https://lifeinthefastlane.com/ecg-library/hcm/
E: Epsilon wave (Arrhythmogenic RV Dysplasia): The RV gets replaced by fibrofatty tissue. Common in people from ITALY. ADMIT for AICD placement. https://lifeinthefastlane.com/ecg-library/basics/epsilon-wave/
B: Brugada: I like to think of it as a downward slash (\) from S to T in V1 and V2. Look at life in the fast lane for some good pictures. Remember, this is an inherited SODIUM channelopathy, seen in young men of Asian descent. ADMIT FOR AICD. https://lifeinthefastlane.com/ecg-library/brugada-syndrome/
@: AV Node Blocks: See above
D: Delta Wave (WPW): Accessory pathway called the BUNDLE OF KENT lets signals bypass the AV node. See a SHORT PR and slurred QRS upstroke giving characteristic DELTA WAVE. Can lead to significant dysrhythmias called Orthodromic and antidromic AV reentrant Tachycardia. Orthodromic is NARROW and MORE COMMON. Treat like AVNRT (Vagal, adenosine, synch cardiovert if unstable). For ANTIDROMIC: it is WIDE and less common but can turn into VFib. AVOID AV BLOCKING DRUGS (no adenosine). Treat with Procainamide or ibutilide if stable, if unstable, SYNCHRONIZED CARDIOVERT.https://lifeinthefastlane.com/ecg-library/pre-excitation-syndromes/
Side note: In case you thought medicine was fair, be aware of Lown-Ganong-Levine syndrome which can present with syncope and has an accessory pathway like WPW, but DOES NOT HAVE A DELTA WAVE. Key to diagnosis is a VERY SHORT PR interval with no delta wave. And some luck.
Q: QT Prolongation: See above
Ok, I’m over Syncope. Let’s talk some Electrolytes and bonus topics:
Hyperkalemia: Think Tall Peaked T wave -> p waves flatten and QRS Widens -> Sine pattern
Hypokalemia: Flattening of the T wave, U wave (following T wave).
Hypercalcemia: SHORT QT, depressed and shortened ST seg, wide T waves
Hypocalcemia: PROLONGED QT (esp with Ca <6)
Digitalis: Can see the digitalis EFFECT which happens to patients on Dig, NOT A SIGN OF TOXICITY: -Scooped ST segments -Short QT intervals -Flat T waves -Prominent U Waveshttps://lifeinthefastlane.com/ecg-library/digoxin-effect/
SIGNS of DIG TOXICITY: PVCs are MOST common, also think dig when you see slow afib (a fib with vent rate <60) or bidirectional VTACH (As above)https://lifeinthefastlane.com/ecg-library/basics/digoxin-toxicity/
Hypothermia: Osborn wave. Yes its silly, but test makers love silly things with little clinical value. https://lifeinthefastlane.com/ecg-library/basics/osborn-wave-j-wave/
Pericarditis:
Stage 1: Diffuse ST elevation (may see ST depression in AvR and V1) with PR DEPRESSION
Stage 2: ST and PR segments normalize, T waves FLATTEN
Stage 3: Diffuse T wave inversion
Stage 4: Back to normal