drugs/electrolytes/ pericarditis Flashcards
EKG changes with digoxin at therapeutic levels
short QT interval
flattened T waves
asymmetric ST depression and T wave inversion in leads w/ tall R waves
coved ST segment (gradual downslope)
prolonged QTc in men
more than 0.44 secs
why do you see AV blocks with digoxin at toxic levels
because it slows the conduction through the AV node
what are the EKG changes with a very low K
prominent U waves
with ___ (drugs) you need to monitor the QT interval and DC the drug if ____
with anti-arrhythmics you need to monitor the QT interval and DC the drug if more than 25% prolongation develops
(or QTc more than 0.5 seconds)
amitryptyline, doxepin, and nortriptyline
what are they and what do they do
TCAs
prolong the QT interval and put pt at risk for V Tach and torsades
narrow QR and wide RS
long PR interval (hidden beneath T)
EKG changes with hypercalcemia
- decreased automaticity
- increased PR interval
- increased QRS interval
- BBB
- AV block
- short refractory period
- short ST segment
- short QT interval
QRS complexes with changing amplitudes
elecritical alternans seen in
LARGE PERICARDIAL EFFUSION
digoxin has a narrow therapeutic window and ___ excretion, so be careful with ___ and ___
digoxin has a narrow therapeutic window and renal excretion, so be careful with geris and CKD pts
prolonged QTc in women
more than 0.46 secs
EKG changes in hypokalemia
flattened T wave
U waves
ST depression
EKG changes in hyperkalemia
tall peaked T waves (tent like)
flattened P waves
1st degree AV block
wide QRS
sine wave pattern
you can differentiate pericarditis from MI b/c the ST elevation is ___ and ____, and _____ is also commonly seen (you’ll also not have weird Q waves)
you can differentiate pericarditis from MI b/c the ST elevation is DIFFUSE and UPSLOPING, and PR INTERVAL DEPRESSION is also commonly seen
prochlorperazine
what is it and what does it do
phenothiazine
prolong the QT interval and put pt at risk for V Tach and torsades
with acute pericarditis, the ST segment ____
evolves: it goes from being elevated to returning to baseline, and the T wave inverts
tall peaked T waves
hyperkalemia
positive inotropy (contractility)
negative chronotropy (HR and AV conduction)
digoxin
delayed repolarization following depolarization
associated with ___
Long QT Syndrome
associated with ventricular dysrhythmias (v-fib and torsades)
arrhythmias associated with exercise
most common thing to see with pulmonary embolism
sinus tachycardia
(esp. if PE is small)
therapeutic drug levels of digoxin
0.8 to 2.0 ng/mL
what are the EKG changes in K over 7.0
sine wave
(wide QRS and peaked T waves become indistinguishable)
short QT
hypercalcemia
digoxin
EKG changes with low electrolytes (K, Ca, Mg)
may progress to
prolonged QT
may progress to V-tach or torsades
you can differentiate benign early repolarization from MI by
(6 things)
- the ST segment will be upsloped (like in pericarditis)
- doing multiple ECGs- the findings will be stable
- no other ischemic findings
- the ST elevation will be minimal (less than 1/4 the T wave height)
- the T wave will be asymmetric
- the J point will be notched
all intervals prolonged (PR, QRS, QT)
osborn waves
arrhythmias
bradycardia
slow a-fib
artifact
hypothermia
(artifact is from shivering)
what are 2 abnormalities you might see with pericarditis with effusion
low voltage in all leads
electrical alternans
EKG changes with PE
sinus tachycardia
S1-Q3-T3
RAD
RAE
RBBB
T wave inversion (V1-4)
lateral S waves
tx for brugada syndrome
ICD
implantable cardioverter-defibrillator
coved ST elevation followed by inverted T wave in leads V1-3
brugada syndrome
effects of digoxin on the body at toxic doses
conduction blocks
tachydysrhythmias
increased risk of renal dz, hypokalemia, aging
syncope
fam hx of sudden cardiac death
asian
in 30s
V-tach
brugada syndrome
downsloping ST segment elevation
MI
____ is a normal finding with elevated, ____ ST segments
BENIGN EARLY REPOLARIZATION is a normal finding with elevated, UPSLOPING ST segments
brugada has ___ types with different ___ abnormalities
brugada has 3 types with different ST elevation abnormalities
QT interval less than 0.35 seconds
short QT syndrome
upsloping ST segment elevation
pericarditis
what leads should you look for brugada syndrome
V1-3
sine wave pattern
merging of S and T waves
seen in hyperkalemia
what are the EKG changes with a slightly low K
T wave flattens
U wave appears
long QT
hypocalcemia
antiarrhythmics
TCAs
phenothiazines
macrolides
ST segment elevation that has an abrupt ascent at the J point and then a plunge back down the the baseline
osborn waves
seen in hypothermia
most characteristic rhythm disturbance with toxic levels of digoxin
PAT with second degree AV block (2:1)
S1-Q3-T3 is seen with
massive PE:
large S in lead 1
deep Q in lead 3
inverted T in lead 3
quinidine, procainamide, disopyramide, amiodarone, and sotalol
what are they and what do they do
(anti-arrhythmics)
prolong the QT interval and put pt at risk for V Tach and torsades
wide QRS
QT interval abnormalitiy associated with syncope, arrhythmias, risk of sudden cardiac death
short QT syndrome
dampened electrical output with low voltage in all leads
+/- T wave and ST segment changes
pericarditis with EFFUSION
the fluid collection dampens the electrical output
toxic blood levels of digoxin
> 2.4 ng/mL
azithromycin, clarithromycin, erythromycin
what are they and what do they do
macrolides
prolong the QT interval and put pt at risk for V Tach and torsades
effects of digoxin on the body at therapeutic doses
slowed SA node and conduction through AV node
parasymp effect
what is QTc
the corrected QT interval:
corrects what the QT would be if the HR was 60 bpm
EKG changes with digoxin at toxic levels
slow HR, fast HR, PVCs
1st, 2nd, or 3rd degree AV block
any tachydysrhythmia
PAT with second degree AV block
what are the EKG changes in K of 5.5 to 6.5
tall, peaked, narrow T waves
