EKG Flashcards
sinus tach
> 100 bpm
if >140-150 (something else going on)
sinus denotes that there is a p-wave
junctional implies absence of p-wave
sinus brady
HR less than 60
atrial flutter
“saw tooth pattern”: flutter/f-waves
comes in specific HRs, (comes with a block)
300/150/75
300: 1:1
every 1 f-wave you are getting a QRS
-v. few things make a HR 300!
150: 2:1 (most common)
2 f-waves for a QRS
-consider a flutter along with sinus tach
75: 3:1
3 f-waves for a QRS
a flutter
rapid succession of identical back to back atrial depolarization waves
identical morphology –> “saw tooth”
tx same as a fib (rate control, anticoag., cardioversion)
definitive tx is catheter ablation: trying to destroy wire? (neural condition) that is causing the arrhythmia
know chart of AVL, V1 etc
on slide
cheat
print out 2x as fast
spread out rhythm
atrial fibrillation
irregularly irregular, Chaotic erratic baseline
no discernable p-waves, Irregularly spaced qrs complexes
usually in response to ventricular response (pulse, HR)
serious if RVR (rapid ventricular response)
a fib slide
FA: HTN, CAD, rheumatic heart disease, *binge drinking (“holiday heart”), HF, valvular disease, *hyperthyroidism
can lead to atrial stasis, CVA, thromboembolisms
worse: in and out of a fib! –>atrial “kick”; feels like worms–>thrombus gets knocked out–>stroke
a fib tx
rate control (B-blockers, β-blocker, non-dihydropyridine Ca2+ channel blocker, digoxin)
anticoagulation (coumadin/warfarin, pradaxa) (may not need based on RAD score)
rhythm control (class IC, III antiarrhythmics)
cardioversion (electrical or pharmaceutical)
what is the concern with a fib with RVR ??
the concern is decreased heart filling (i.e. HR 160)
hypotensive (BP dec.)
if use B-blocker to lower HR, problem: exacerbate hypotension (often still use with hope that lowering HR increases filling time, eventually inc. BP)
ST depression in lateral leads
oxygen delivery to heart is sacrificed: rate-related ischemia
-reversible, need to slow down HR
pericarditis
inflammation of heart sac
disease of younger ppl
EKG changes: diffuse ST segment elevation
looks like a “global MI”: systemic problem
KEY: PR depression
dips below baseline
Superventricular tachycardia: SVT
HR 160-170, can be as high as 210, 220
palpitations, SOB, syncope, lightheadedness, etc.
can’t make out p-waves
regular rate (vs. afib)
rate-related ischemia:
ST depression
when rhythm interrupted: adenosine was given, or other mechanisms to stop SVT
how do you stop SVT
bear down
or carotid massage 1 side
adenosine: will stop heart, unpleasant experience, CP, SOB
- warn them: will feel like you are going to die
if pressure of 80: shock him!
“edison medicine” (unstable pt)
how to tx hyperkalemia w/ EKG changes
**calcium: does NOT lower K+ BUT stabilizes cardiac membrane
second: lower K+ with insulin IV
then dextrose to avoid hypoglycemia
more K+ lowering drugs:
albuterol bicarb Kayexelate (sucks!) causes diarrhea, intenstinal ischemia, necrosis (does not lower K+ much! dead drug)
hyperkalemia on EKG
peaked T-waves
similar to early MI (hyperkalemia more common)
will increase if exacerbated/prolonged
severe hyperkalemia
widened QRS (bad!!! always)
peaked T waves
PR prolongation
near sinusoidal pattern–>seconds to live
give Ca2+!!! can see QRS narrowing
if all drugs not working in hyperkalemia ??
why does this happen??
dialysis
stopped taking diuretic, still K+
noncompliant with dialysis, renal diet
V tach
varying presentation
AV dissociation
stable:
A/O, mild symptoms, stable vitals besides tachy, no resp distress, have time!
-tx: drogas
unstable:
hypotensive, confused, lethargic, dead
-tx: shock
tx differently!
can’t tell from EKG
torsades de pointe
near death, very serious rhythm
polymorphic vtach
sinusoidal waveform
*long QT interval is huge risk factor
can lead to vfib: DEAD!
causes:
drugs, (that inc. QT: macrolides: azithromycin, erythromycin; zofran) (more to come)
low K+, low Mg+
tx: Mg sulfate
if K+ continually low even with tx, check Mg level
which drugs cause long QT (can lead to torsades)
ABCDE
antiArrhythmics (class 1A, III) antiBiotics (macrolides) antiCychotics (haldol/haloperidol) antiDepressants (TCA's: narrow window) antiEmetic (zofran/ondansetron)
congenital long QT syndrome: inherited
Romano-ward syndrome:
autosomal dominant, pure cardiac phenotype (no deafness)
Jervell and Lange Nielsen syndrome:
autosomal recessive and sensorineural deafness
congenital long QT syndrome: others
repolarization abnormality (ion channel defects)
inc. risk of sudden cardiac death due to torsades de pointes
1st degree AV block, sinus bradycardia
PR >200 msec (prolonged)
asymptomatic, benign
2nd degree type 1
mobitz 1
usually asymp, regularly irregular
PR lengthens then QRS drops! :at least you saw it coming (less sev.)
