Cards

Bradycardia: HIDE = Hypothermia/Hypothyroidism, Ischemia/Infection (sepsis), Drugs (BB, CCB, Dig), Electrolytes (hyperK)

Lead reversal: if P and T inverted in same lead

Nomenclature: first 3 letters most important
Screen Shot 2017-11-09 at 7.29.32 AM
http://www.cardiacengineering.com/pacemakers-wallace.pdf

-“overdrive pacing” for torsades or VT = pacing over the rate of the underlying bradycardia which led to the transient monomorphic or polymorphic VT
–mechanism: bradycardia accentuates QT prolongation –> incr dispersion of refractoriness –> R on T phenomenon –> promotes re-entrant circuit (in ventricle)
–same theory for bigeminal PVC formation (“rule of bigeminy”) – the bradycardia in this case is the compensatory pause after the PVC
-stable VT – give 4-6 Gm Mag (goal level >4)

afib and aflutter pts syncopize when convert back into NSR (due to a sinus pause that represents abnormal sinus recovery time) = “tachy brady syndrome,” a type of sick sinus syndrome
-aflutter is difficult to control medically, but responds well to cardioversion (even at low joules)

Diuresis in CHF:
-if pt has poor systolic LV function (low EF) at baseline and presents in pulmonary edema with soft BP, a decrease in preload (diuresis, nitroglycerin) may actually increase CO or at least keep it more or less the same (image below: B –> C)
Screen Shot 2017-11-04 at 2.55.15 PM

Impella = intravascular LVAD
—unlike IABP or VA ECMO, it sucks out volume from LV / unloads the LV -> greatly improving forward flow and preventing backward flow

-the lead most likely to show ST changes = V5 (bc all coronaries have lateral tributaries)
Screen Shot 2017-11-04 at 3.11.36 PM

to diagnose complete heart block, all P waves must march out on time and all QRS complexes must march out on time
-1st degree AV block – can occur either at the AV node or between the SA node and AV node
-posterior fascicle is short and thin, thus much harder to knock out

VT vs SVT with aberrancy or underlying BBB: Brugada criteria, Vereckei criteria
—VT: fusion beats and escape beats (sinus-originating impulses coming through)
—regular
—precordial leads all (+) or all (-)
—RSr’ in V1 – like in RBBB, except first R is larger than second

Management of stable VT: amio push +/- drip, lidocaine push +/- drip, procainamide

-SVT (ex afib) with aberrancy: irregular, old RBBB or LBBB -> beta blocker ok

LVAD indications: cardiogenic shock with forward function refractory to medical therapy, EF <30%???
LVAD complications: infection, thrombosis (causing hemolysis, incr pump power required to maintain flow), dysrhythmias (postsurgical scarring), GIB (AVMs and acquired vWF), low battery, hypotension to MAP<60 (these pts very preload-dependent), high afterload to MAP>90 (obstruction or HTN, if latter choose ACEI or BB), suction event
–exam: precordial “hum” rather than S1/S2, no pulses
–obtain MAP by manual BP = pressure reading when Doppler flow becomes audible
-absence of hum = pump failure
-use relative sizes of RV and LV on echo to narrow differential
-LVAD pts can have walking vfib with fatigue as their only symptom, but will eventually develop heart failure. Give iv amio, lidocaine, procainamide. May cardiovert or defibrillate
-If pt becomes unresponsive with poor perfusion, must begin CPR

Critical Ao stenosis = area <1cm
-these pts have a fixed CO and cannot increase it in compensation
—are at risk of syncope, cardiogenic shock, LV ischemia (hypertrophic wall) and pulmonary edema
—go easy on fluids if pt not crashing
—avoid hypotension bc pts cannot compensate
—avoid any increase in myocardial demand, as pt is at risk for LV ischemia as it is
-these pts need rhythm control if in afib – their LV relies on atrial kick for sufficient filling in diastole
-phenylephrine is vasopressor of choice, norepi is 2nd line
-intubation is high risk given hemodynamic effects of induction agents and positive pressure ventilation – optimize preload prior, have phenylephrine pushes ready, and consider placing A line if there is time

first MI in little old lady – high risk of complications, incl cardiogenic shock, septal wall rupture, free wall rupture, etc. Will need central line and arterial line

How to use axis deviation:
Left Axis Deviation: LAD from VILLA = VT, Inferior wall MI, LVH, LAFB, LBBB
Right Axis Deviation: RAD RALPH = RVH, Anterolateral wall MI, LPFB (hemiblock)
*note that RBBB will NOT cause a coronal axis deviation bc the RV contributes little to the net vector of myocardial depolarization

Bundle Branch Blocks – QRS > 120ms (if <120ms, considered “incomplete” BBB)Screen Shot 2017-11-12 at 11.47.35 AM
RBBB = rSR’ in V1-V3 (right heart leads) that is “M” shaped + widened S wave in V5-V6 (& lateral limb leads)
—R’ = delayed RV depolarization due to the block
no change in coronal or precordial axis as the RV contributes little to the net vector of myocardial depolarization
—V1-V3 have associated T wave inversions
—note that the 2nd R wave is larger than the first, unlike in VT
if V1-V3 also have a humpback appearance, it is Brugada syndrome!
Screen Shot 2017-11-12 at 12.03.38 PM

LBBB = widened S wave in V1-V3 + notched R wave in V5-V6 that is “M” shaped (& lateral limb leads)
—the latter aspect of notched R wave in V5-V6 = delayed LV depolarization due to the block
—left axis deviation (coronal axis) & poor/delayed R wave progression (precordial axis deviation – net vector moves toward RV)
—“appropriate discordance” = the ST segments and T waves point in the opposite direction to the main vector of the QRS complex

How to use R wave progression (precordial axis deviation):
*normal = R > S wave by V4
early R wave progression: posterior wall MI, LPFB???
poor/delayed R wave progression: anterior wall MI, LAFB???, LBBB
*note that RBBB will NOT cause a change in R wave progression bc the RV contributes little to the net vector of myocardial depolarization

Screen Shot 2017-11-12 at 11.33.01 AM.png
*Ant fascicle = anterior & toward right side of LV????
*Post fascicle = posterior & toward left side of LV????

Don’t Miss EKGs
posterior wall MIs: ST depressions in V1, V2, large R waves
—place posterior leads V7-V9
Screen Shot 2017-11-12 at 11.10.35 AM

-**for both inferior and posterior MI, determine whether or not the RV has infarcted
—STE in III > II
—obtain right sided leads…or can just place V4R (opposite of V4), which is most sensitive
–these pts are preload dependent – needs fluids, no nitro or morphine. May have JVD (RV failure) and hypotension

-Wellens: biphasic T

High Risk EKGs

Wellens Syndrome

  • deeply inverted or biphasic T waves in V2-3, which is highly specific for a critical stenosis of the left anterior descending artery (LAD).
  • Patients may be pain free by the time the EKG is taken and have normally or minimally elevated cardiac enzymes; however, they are at extremely high risk for extensive anterior wall MI within the next few days to weeks.

https://lifeinthefastlane.com/ecg-library/wellens-syndrome/

aVR Elevation

  • Widespread horizontal ST depression, most prominent in leads I, II and V4-6
  • ST elevation in aVR ≥ 1mm
  • ST elevation in aVR ≥ V1

Screen Shot 2017-08-25 at 10.29.36 AM

ST elevation is aVR is postulated to result from two possible mechanisms:

  • Diffuse subendocardial ischaemia, with ST depression in the lateral leads producing reciprocal change in aVR due to a process causing generalized coronary ischemia (triple vessel disease, post cardiac arrest)
  • Infarction of the basal septum, i.e. a STEMI involving aVR. aVR records electrical activity from the RVOT and the portion of the septum closest to the base (supplied by a proximal branch of the left main)

https://lifeinthefastlane.com/ecg-library/lmca/

VT vs block with tachycardia:
Screen Shot 2017-08-25 at 2.38.45 PM

Screen Shot 2017-08-25 at 3.07.25 PM.png

Anomalous left coronary artery from pulmonary artery syndrome –> SCD

magnet –> converts pacemaker to fixed rate pacing