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.)
2nd degree type 2
mobitz 2
QRS drop without lengthening PR
tx: pacemaker
frequent, random dropping
present with syncope due to lack of cardiac output
FA: may progress to 3rd degree block
3rd degree block
QRS: HR in 30s!
miscommunication btw SA and AV node (intrinsic, slower)
p-waves: all march out (i.e. HR 70)
ZERO relationship btw p waves and QRS
atrial rate faster than ventricular rate-bradycardic rhythm (not sinus bradycardic: p-waves not influencing QRS)
3rd degree HB tx
can often be caused by ??
tx: pacemaker needed
often v. symptomatic
lyme disease can cause this
RBBB
QRS > 100?
“bunny ears”: V1, V2, V3 (rSR’)
V4, V5, V6: wide S wave
typically asymptomatic
may be acute (rare)
from scar tissue from HA, infection, etc
LBBB
more worrisome than RBBB
V6: broad R wave with deep S, inverted T-wave
V1, V2, V3: QS pattern
cannot dx acute MI in LBBB
QRS > 120 mS
need previous EKG to dx this over STEMI:
STEMI unless proven otherwise
page cardiologist
STEMI
ST elevation MI
“tombstone”
some cardiologist require
reciprocal changes:
ST segment depressions
T-wave inversions:
further support MI
inferior wall MI
II, III, aVF
reciprocal changes in 1, aVL, V2
anterior wall MI
“the widow maker”
V2, V3, V4, V5
reciprocal changes: aVR ??
occlusion of LAD, supplies largest part of heart
the more proximal, the more damage
why do ppl die of heart attack?
lethal arrhythmias
necrosis –>source of arrhythmias
anterior wall MI: don’t confuse with ??
hyperkalemia!
Brugada syndrome
autosomal dominant
asian, mostly male (8:1)
pseudo RBBB
ST elevation V1-V3 (all the time, not a STEMI)
inc. risk of ventricular tachyarrhythmias and sudden cardiac death
no known CAD or structural abnormality
Brugada syndrome tx
implantable cardioverter-defibrillator (ICD)
about 75% increase in survival? (dec. in morb/mort)
Vfib
completely erratic rhythm
no waves of any sort
fatal if no immediate CPR/defibrillation
(DEAD)
rhythm you go into before death
reasoning behind ??? everywhere
Vfib and Vtach
AEDs
inferiolateral ischemia
oxygen deficiency to inferiolateral area
analogous to penumbra in stroke (dead area is necrosis)
-is reversible, can save!
how to fix??:
find the source
i.e. unstable angina (CAD pre-MI)
how to ID inferiolateral ischemia
ST segment depression (acute! typically) -dynamic
inferior: II, III, aVF
lateral: V5, V6
ddx from ST depression/T-wave inversion caused by from CAD (can be acute or old!)
WPW: Wolff-Parkinson White
most common type of ventricular pre-excitation syndrome
abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) BYPASSES rate-slowing AV node
ventricles begin to partially depolarize earlier as seen via delta wave and wide QRS and short PR
may result in reentry circuit–>SVT (what kills!)
WPW tx
NO DIGOXIN, NO B-BLOCKERS, NO CCBs
T-wave inversion lateral leads (ischemia)
inversion: V2, V3, V4, V5, V6 ?
slide 86: inferior MI, anything else??
what vessel occluded in inf. MI
RCA : may also lead to posterior MI
posterior wall MI
- (often) in conjuction with inferior wall MI
- ST depression in V1 or V2 (back of heart)-OPPOSITE/RECIPROCAL of anterior wall MI (so depression vs elevation)
* flip around and read thru back, will look elevated*
LAD artery in MI
anterior wall MI (V1-V4)
anteroseptal (V1-V2)
anteroapical (V3-V4) (distal LAD)
LCX (circumflex) or LAD in MI
anterolateral (V4-V6)
LCX in MI
lateral wall (I, AVL)
RCA in MI
inferior wall (II, III, AVF)
inferior wall MI (RCA) will present with what type of symptoms ??
GI symptoms: epigastric pain, N/V
*don’t miss!
how to tx MI
ASA
plavix (clopidogrel)
(both decrease morb/mort)
nitro? (does not dec. mort/morb) will make feel better
actually give first! works quickest to decrease preload
don’t give nitro to pt w. ??
inferior wall MI
RV responsible for pre-load, if knocked out, exacerbates decreased pre-load, weakens pump
ECHO: of MI shows: wall motion abnormality, hypokinesis
give morphine
