Potpourri-ECG

Eponyms & Nice-to-knows

Af with WPW

aVR

BER vs MI

LBBB

Posterior MI

RBBB

VT vs SVT

Eponyms

Ashman Phenomenon

RBBB in AMI = pLAD

Ashman Phenomenon: usually in Af, a wide QRS, usually an RBBB, that terminates a short cycle that follows a long cycle (long R-R). link/photo/pdf

"the earlier the PAC occurs in the cycle, and the longer the preceding cycle, the more likely the PAC will be conducted aberrantly"

- because the longer the preceding cycle (the slower the heart rate), the longer the refractory period, therefore the PAC terminating the short cycle. occurs in the refractory period, hence, it will be aberrant (wide).

therefore occurs in long-short cycle, but even more common in short-long-short cycle.

Right Bundle recovers slower (longer refractory period) then Left Bundle, that's why the most likely from is RBBB.

-----

Fisch criteria to differentiate from ventricular ectopic.

Wikipedia: It occurs because the duration of the refractory period of the myocardium is proportional to the R-R interval of the preceding cycle. A short R-R interval is associated with a shorter duration of action potential and vice versa. A long R-R cycle will prolong the ensuing refractory period, and if a shorter cycle follows, the beat terminating the cycle is likely to be conducted aberrantly. Because the refractory period of the right bundle branch is longer than the left, the right bundle will still be in the refractory period when the supraventricular impulse reaches the His-Purkinje system, resulting in a complex with right bundle branch morphology.

RBBB in AMI = pLAD

- because R bundle is supplied by first septal perforator which is the most proximal branch of LAD (usually that is, sometimes it arises after D1, but usually before D1)

- RBBB in AMI is also a poor prognosis

Drug Mixing/Nursing

Amiodarone (link)

- 150mg/3mL per vial

—FIRST 24 HOURS—

Loading infusions
First Rapid:	150 mg over the FIRST 10 minutes (15 mg/min). Add 3 mL of amiodarone I.V. (150 mg) to 100 mL D5W (concentration = 1.5 mg/mL). Infuse 100 mL over 10 minutes.
Followed by Slow:	360 mg over the NEXT 6 hours (1 mg/min). Add 18 mL of amiodarone I.V. (900 mg) to 500 mL D5W (concentration = 1.8 mg/mL).
Maintenance infusion	540 mg over the REMAINING 18 hours (0.5 mg/min). Decrease the rate of the slow loading infusion to 0.5 mg/min.

After the first 24 hours, the maintenance infusion rate of 0.5 mg/min (720 mg/24 hours) should be continued utilizing a concentration of 1 to 6 mg/mL (amiodarone I.V. concentrations greater than 2 mg/mL should be administered via a central venous catheter). In the event of breakthrough episodes of VF or hemodynamically unstable VT, 150 mg supplemental infusions of amiodarone I.V. mixed in 100 mL of D5W may be administered.

Such infusions should be administered over 10 minutes to minimize the potential for hypotension. The rate of the maintenance infusion may be increased to achieve effective arrhythmia suppression.

RBBB

Diagnostic criteria (link)

Broad QRS > 120 ms

RSR’ pattern in V1-3 (‘M-shaped’ QRS complex)

Wide, slurred S wave in the lateral leads (I, aVL, V5-6)

LBBB

1. QRS > 120 msec (110 - 119 = incomplete)
2. no Q, monophasic R in I and V6
3. QS or rS in V1

Source

Marriott's Practical Electrocardiography. 11 ed. 2008.

Af with WPW

3 Things:

1. Rate 300/min (R-R is one big square)
2. Wide QRS
3. Irregularly-irregular

VT vs SVT

Differentials of WCT
SHIT (usually these are slower <100-120/min)
STEMI with massive ST
Hyperkalemia
Idioventricular, accelerated
Tox TLCDD (TCA, Lithium, Cocaine, Dig, Diphenhydramine]
Pacemaker-Mediated Tachycardia

VT vs SVT with abberancy

Clinical
- unstable = sync CV
- the older the age, the more it's VT
- Hx ACS/CHF/CMP/ICD
- young patients, if not sure, treat as VT

Seven Things = only look here if patient is stable
1. old ECG: (eg if known RBBB, likely SVT)
2. check P waves before QRS = don't miss sinus
3. RBBB and LBBB is clearly identified = SVT
4. FACC: Fusion beats, AV dissociation, Capture beats, Concordance
5. QRS duration: VT >140ms/3.5small sq (except fascicular VT or RBBB + leftward axis), the longer the more it's VT
6. check R wave of V1, look for subtle notching = could be P wave = AV dissociation
7. Algorithms: Brugada, Vereckei, aVR (Vereckei 2), Sasaki

Sasaki
1. initial R in aVR
2. longest RS ≥100 ms (2.5 small squares) in any precordial leads
3. initial r or q ≥40ms (1 small square) in "any" lead

Others:
- R or qR pattern on V1 = VT
- frontal QRS axis between 180 and 270 degrees = VT (ERAD)
- LBBB + Right axis deviation = VT
- RBBB pattern when present in the native sinus rhythm = SVT
- varying BBB = SVT
- rsR' pattern in V1 = SVT
- ectopic P wave preceding the dysrhythmia = SVT

- If there is a transition from narrow to wide, is the rate the same? then it must be SVT.

Algorithms:

1. Brugada
2. Vereckei
3. aVR (Vereckei 2)
4. Sasaki = simplest, and most superior (?)

Step 1: Initial R in aVR?
If yes, then rhythm is VT. If no, step 2.

Step 2: Interval from onset of R wave to the nadir of the S ≥ 100 msec (0.10 sec) in any precordial leads?
If yes, then rhythm is VT. If no, step 3.

Step 3: Initial r or q ≥ 40 ms in any lead?
If yes, then it is VT.
If no, then it is SVT

If still uncertain and patient is stable, handover to next shift

Links:

http://lifeinthefastlane.com/ecg-library/basics/vt_vs_svt/

Posterior MI

Posterior MI

• ST depressions, most markedly in V1-3
• Upright R wave on V1-3
• Tall T waves on V1-3
• prevalence: 3-11% of all STEMIs (about 8%)

vs Subendocardial Ischaemia: ST depressions most prominent in V4-6

Link: Dr Smith ECG

aVR

aVR: Importance (mostly ignored, why)
In theory, aVR looks at the R upper side of the heart (RV outflow tract and basal septum). In practice, aVR is only regarded as a reciprocal reflexion of the L lateral side of the heart which is already covered by aVL, II, V5, 6 = therefore ignored

• sinus rhythm
• origin of arrhythmia: (+) P wave = SVT; (-) P wave = VT (note: P wave is hard to find in WCT, besides, it can also be mistaken for artifact)
  check AVR Algorithm
  
• unstable angina + at least 8 leads of ST changes + ST elevation aVR = LMCA or TVD
• PE: ST elevation (RV overload)
  
• proximal LAD
• TCA poisoning, upright aVR
• pericarditis: PR elevation (+ PR depression the rest of the leads