12 Leads - Semester1 Flashcards
What is this rhythm ?
What would be your treatment approach / choices ?
Second Degree Type II (4:1) (consistent PRI……but looks borderline 3rd degree….but overall….most of the complexes with P and QRS appear to have a consistent(ish) PRI - - - there was some reasonable debate on this , but answer is Second Degree Type II)
Tx : expect deterioration to 3rd degree or worse. Treatment is Pacing as main option.
However, some may consider ISOPROTERONOL (which only acts on B, so won’t increase atrial rate, just ventricular rate) IF AND ONLY IF the patient is Hemodynamically Stable (as Natalie describes as comfortable at rest, BP ok, maybe a little dizzy or SOB with activity). This approach not commonly used throughout Ornge, but - seems to be an approach in GTA if trying to avoid pacing if possible (pain / patient comfort and hassle)
Aside:
ISOPROTERONOL dosing as per MDSO (supplied 0.2mg/mL in either a 5 mL (1mg/5mL) or 10 mL (2mg/10mL)
AV Block Dose: 200mcg/1mL SC or IM initially, followed by another 150 -200 mcg SC or 20-1000 mcg IM depending on clinical response
If IV Access available and emergency “IV Direct”, then use 40-60 mcg. (dilute 0.2mg/mL to 10 mL in NS or D5W to
produce 0.02mg/mL - - inject at max rate of 1mL /min (0.02mg/min).
pg 124 of MDSO for more info.
Interpret this 12 Lead. What is the clinical significance
1st degree, PRI long (>0.20)
Not really an issue, due to increased vagal tone, sometimes seen in athletes , or old MI
Interpret this Rhythm.
Second Degree Type II (consistent PRI)
*not the most obvious, can also look like at Type I (longer longer drop) in some places…..but the official answer is type II according to Britton in Lab.
A middle age male c/o CP and syncopal episodes presents with this ECG. Interpret the rhythm.
After a while at the hospital he deteriorates and you see the second ECG. Interpret that. What is the needed treatment?
1st ECG = RBBB with LAFB and also a 1st degree block
2nd ECG = RBBB with LAFB and also a 3rd degree block, needs PACING as Tx
The LAFB is function of RBBB + LAD - - - but need to compare to I,II,III/aVF - - -as I and aVF alone chart not enough here.
the RBBB with Bunny Ears in V1 is wide enough to call it a RBBB, but other criteria include Slurred S wave in I and V6
If you had a TACHYdysrythmia with Hypotension, what Vasopressor would you consider ?
Phenylephrine
(all alpha, no Beta) - so only increase BP without increasing HR…..also one of it’s side effects is “reflex bradycardia” ( I think due to sudden change in baroperception in heart and aortic arch ? )
This was from a case study we skipped in Lab 2 that was to be about a Tachy Rhythm and choice of vasopressor…..because we were running low on time, but based on the actions on vasopressors, Only 2 vasopressors have no Beta effect : Phenylephrine and Vasopressin. Vasopressin is not safe for peripheral use, whereas Phenylephrine is. So based on that - and my judgment this is probably the right answer.
Interpret this rhythm. What is the expected treatment.
Classic Monomorphic VT
Step 1 of Brugada : unable to distinguish between R and S…..so, it’s VT
This person is about to go into cardiac arrest, even if has a pulse, cannot do synchronized cardioversion, no R waves to track - - - so this person needs rapid defibrillation (even alive ? I think so - but maybe double check with instructors)
Interpret this Rhythm.
Bigeminy with Long QT and causing R on T.
High Risk for Torsades dt RonT
Long QT often a result of malnutrition and lack of Mg++
Interpret this Rhythm.
Torsades (Polymorphic VT)
Requires Mg++ as part of the treatment
A elderly, homeless patient arrives at hospital in the first rhythm, then deteriorates into the second ECG. Interpret both the ECG.
What personal factors does this patient have that contribute to this these rhythms?
What kind of treatment would you consider ?
1st Rhythm = Bigeminy with Rapid Ventricular Response (with long QT and RonT : note Long QT = <0.4 (two big boxes from Q to end of T)
2nd Rhythm = Torsades (Polymorphic VT)
Malnutrition, low Mg++, increases risk of long QT, which in turns risks R on T which in turn risks Torsades, some antibiotics can also cause low Mg++
Tx: Defib needed, won’t be able to synchronize…..then if Torsades terminated , need to replace Mg++…..most likely also need to replace K+ (see labs for K+, Mg++ not usually reported). If Mg++ is low, usually K is low too.
ASIDE…….”Previous articles suggested that impairment of Na-K-ATPase caused by magnesium deficiency contributes to K+ wasting.3,4 Magnesium deficiency impairs Na-K-ATPase, which would decrease cellular uptake of K+.3 A decrease in cellular uptake of K+, if it occurs along with increased urinary or gastrointestinal excretion, would lead to K+ wasting and hypokalemia. Little K+ is excreted by the gastrointestinal tract normally; therefore, hypokalemia in magnesium deficiency is likely associated with enhanced renal K+ excretion.”
How do you look for a long QT and what is it often related to ?
Long QT = > 0.4 ms (2 big boxes) , measured from beginning to Q (or if no Q, just before R begins, at isoelectric) to end of T
Can be related to low Mg++ from causes such as malnutrion (think homeless etc…)
What would you look for on ECG for Digoxin Toxicity when stable, then when it deteriorates?
Stable rhythm look for “Scooped T’s” (like a U shape after the QRS) in conjunction with PMHx suggestive of Digoxin as a potential medication.
Deterioration : “Classic DIG TOX” = Rapid Artial (A fib or flutter), Slow Ventricular Response, and sometimes difficult to see, but 3rd degree block, as DIG blocks AV completely, so look for interrupted flutter waves by a QRS, where the QRS is very slow.
Identify this Rhythm, What is the most likely cause of it ?
Bidirectional VT.
Rare presentation, but Digoxin Toxicity is the classic cause. (but also Hypokalemia, Catecholamine Induced VT and a few other reasons)
2 QRS complexes alternate, different morphologies, but both WIDE (>0.12) therefore of Ventricular Origin.
Identify this rhythm.
Bidirectional VT
Identify this rhythm.
Bifascicular Block (most common one) = RBBB + LAFB (identified by LADeviation on a RBBB) - not usually a critical finding.
Identify this rhythm
Bifascicular Block : ie RBBB + LPFB (= RBBB + RADeviation) - less common that the one with a LAFB (RBBB with LAD)
Identify this rhythm and estimate the rate.
Sinus Bradycardia. Estimate rate of approx: 37
It’s 8 big boxes away……so 300 , 150, 100, 75, 60, 50, 43, 37
Left Axis Deviation will show what in Lear I, II, III/avF ?
2 options: 0 to - 30 : I = positive, II = equi, III/aVF = negative (Physiological)
-30 to -90 : I = positive, II = negative, III/aVF = negative (Pathological)
