Advanced EKG Flashcards
The more leads…
the more specific the findings
3-lead EKG
single view of the heart’s electrical pattern; only able to monitor one lead at a time
5-lead EKG
multiple views; able to monitor in two or more concurrent leads at once
Lead I, II, & III tracing
upright
How to confirm Asystole in the OR
confirm in a second lead (might have just fallen off)
Recommended lead of choice for electrical cardioversion
Lead II
Lead III gives a better view of
the left ventricle
The purpose of the EKG dictates the…
lead placement
Lead III baseline…
wanders up and down d/t the positive electrode being located on the diaphragm
Best pt position for EKG
supine
Ways to optimize EKG
shave hairy chests, place in proper place around large breasts, dry skin, use alcohol to make it sticky
What should you not use to help leads stick?
deodorant (arid extra dry, ban roll on)
How many electrodes do 12-lead EKGs use?
10 electrodes; one on each limb, six on left chest
Avoid putting leads on
bony prominences (shoulders)
V4 is placed
Mid-clavicular
V5 is placed
Anterior axillary
V6 is placed
Mid-axillary
Inferior Leads
II, III, avF
Septal Leads
V1 & V2
Anterior Leads
V3 & V4
Lateral Leads
V5 & V6
I & avL (high lateral)
RSR prime complex indicative of
RBBB in lead MCL1
Two reasons J-point is important
it is the point of reference for determining BBB & for measuring ST elevation/depression
Rapid axis is used to diagnose
Hemiblocks
Axis =
predominant flow of electricity through the heart (V2)
What do we look at for ventricular axis
QRS complexes
Normal Axis
0-90 degrees; positive in all three leads
Physiological Left Axis Deviation
0 to -40 degrees;
Lead I = positive
Lead II= either
Lead III = negative
Pathological Left Axis Deviation & associated block
-40 to -90 degrees;
I = positive
II = negative
III = negative
Anterior hemiblock
Right Axis Deviation & associated block
90-180 degrees;
I = negative
II = either
III = positive
Posterior hemiblock
Extreme right axis deviation
-90 to 180 degrees;
all negative deflections;
ventricular in origin
causes of LV hypertrophy
HTN, extreme exercise, aortic disease, obesity
causes of RV hypertrophy
severe lung disease
pulmonary valve disease
PE
is a right axis deviation physiological or pathological in adults?
pathological
bundle branches facilitate
syncytium = both ventricles contracting in sync
QRS in BBB
must be wider than .12 seconds (120 milliseconds) or 3 little squares
BBB is a great risk factor for
CHB
BBB negatively affects
contractility
BBB in setting of acute MI
4 times higher mortality rate
Do NOT give Lidocaine (or procainamide) to someone with
BBB in setting of acute MI
Bifascicular blocks
3 types of bifascicular blocks
RBBB + Anterior Hemiblock
RBBB + posterior hemiblock
LBBB (bifascicular all by itself)
type of QRS complex with hemiblock
Narrow
if you say block two different times in a diagnosis…
the patient is at high risk for CHB
High LBBB takes out
both anterior and posterior
RCA supplies blood to
Posterior & inferior LV
Right ventricle
SA & AV nodes
Posterior fascicle of LBB
RCA blocks present as
bradycardia, heart block, elevated CVP, JVD, poor lung perfusion
LAD supplies blood to
Anterior wall of LV
Septal wall of LV
Bundle of His
bundle branches
“widow maker”
Circumflex supplies blood to
Lateral wall of LV
*SA & AV nodes
*Posterior wall of LV
Meds to interrupt atherosclerotic plaque formation
heparin and aspirin
posterior MI presents as
back pain (same as AAA)
Arterial clots present as
cold, ischemia, pain, loss of pulses
PE presents as
SOB, hypoxia, AMS, air hungry, abdominal pain
AMI interventional plan
O2, nitro, pain control, ASA/heparin
percentage of MIs missed on an EKG
50%
MI triad
history, physical exam, EKG
Time and extent of necrosis after MI
30 mins - 10%
1 hour - 30%
2 hours - 50%
3 hours - 60%
6 hours - 90%
24 hours - 100%
Presentation of ischemia
symmetrical inverted T waves in 2 or more related leads
(normal for T-wave to be inverted in lead III & MCL1)
Presentation of Injury
ST elevation in two or more related leads
greater than 1mm
ST depression in the absence of ST elevation
ischemia or subendocardial injury
drug and electrolyte problems - digitalis & hypokalemia
Presentation of infarction
pathologic Q waves (>40 ms wide or 1/3 depth of R wave height) and ST elevation
death or necrosis of tissue
Pathologic Q wave without acute changes
“old” or age undetermined infarction
Inferior (blood supply, leads and reciprocal)
RCA
II, III, aVF
I & aVL
septal (blood supply, leads and reciprocal)
LAD
V1 & V2
no reciprocal leads
anterior (blood supply, leads and reciprocal)
LAD
V3 & V4
II, III, aVF
lateral (blood supply, leads and reciprocal)
Circumflex
V5 & V6; I & aVL (high)
II, III, aVF
Posterior (blood supply, leads and reciprocal)
RCA
V8 & V9 (R>S in V1)
V1-V4 (ST depression)
Right ventricle (blood supply, leads and reciprocal)
RCA
V4R
no reciprocal leads
Most common detected MI
inferior
(50% have posterior and RV involved)
Presentation of inferior MI
Brady, hypotensive, nausea
1st degree HB or 2nd degree type 1
Do you use nitrates with inferior MI
First fluids; use nitrates with caution because RV infarction is pre-load dependent
What type of EKG should be ran if suspected RCA occlusion
15-lead
Most lethal MI
Anterior
can suddenly develop CHB, VT/VF
Who do we need to immediate place combo pads on?
BBB + Anterior wall MI
Anterior MIs can extend to
septum and/or lateral
What do you give for anterior MI?
Nitrates; fluid spared
Infarct imitators
LBBB
LV hypertrophy
Disecting thoracic aorta aneurysm
Pericarditis
Pericarditis
ST elevation in all leads with NO reciprocal ST depression
Pt feels better when they lean forward
Flu-like symtpoms
Dissecting Thoracic Aortic Aneurysm
dangerous if missed diagnosed as MI - do not want this patient getting heparin
NO reciprocal changes
Do you give nitrates to DTAA?
with caution, if at all, d/t heart’s attempt to compensate for decreased after load by increasing HR and contractility causing undue stress on a weak area of aorta
