Lecture 8 Flashcards
inflammation of pericardium
pericarditis
EKG changes in pericarditis
- T wave initially upright and elevated but inverts during recovery phase
- elevated ST segment (flat or concave)
- ST changes diffuse
low voltage seen in all leads
pericardial effusions
electrical alterans
manifested by changing aamplitude of the QRS complex (seen with large pericardial effusions because the heart may rotate freely)
acute occlusions of the pulmonary artery
pulmonary embolism
what rhythm is commonly seen with pulmonary embolism?
sinus tachycardia (esp. if embolism is small)
EKG pattern seen with massive PE
S1 Q3 T3
axis deviation with PE
right axis
other EKG changes with PE
signs of RAE, RBBB, inverted T waves in precordial leads
congenital condition with delayed repolarization following depolarization
long QT syndrome
long QT syndrome is a/w which ventricular dysrhthmias
V. fib and torsafes
-usually a/w exercise
short QT syndrome is a/w?
syncope, ventricular arrhythmias, risk of sudden cardiac death
represents depolarization and repolarization but it is corrected for the heart rate
QTc interval
signs of hyperkalemia
- tall, peaked T waves
- flattened p waves
- 1st degree AV block
- wide QRS complexes
- sine wave pattern (K>7.0)
signs of hypokalemia
- flattened T waves
- appearance of U waves**
- ST segment depression
hypercalcemia will result in ____ (increased, decreased) automaticity with _____(faster, slowed) conduction
decreased; slowed
QT interval for hypercalcemia
shorter!
-short refractory period
QT interval for hypocalcemia
longer!
hypocalcemia can precipitate what?
V. tach or torsades
what ions does digoxin affect the movement of?
sodium and calcium
- slows influx of sodium
- increases influx of calcium
what is the primary biomechanical mechanism of action of digoxin?
inhibition of the Na/K ATPase of the cell membrane
effect of digoxin on contractility and heart rate?
increases contractility and slows heart rate/AV conduction
digoxin effect
expected EKG changes and do not indicate a need to d/c the drug
- seen in therapeutic drug levels
- slows SA node and conduction through the AV node
digoxin therapeutic drug levels
0.8-2.0 ng/ml
toxic blood levels of digoxin
> 2.4 ng/ml
EKG findings a/w toxic blood levels of digoxin
conduction blocks or tachy-dysrhythmias
increased risks a/w toxic blood levels
renal disease, hypokalemia, and aging(?)
Specific EKG changes with therapeutic digoxin levels
- shortened QT interval
- flattened T waves
- asymmetric ST depression and T wave inversion in leads with tall R waves (gradual downslope of ST segment)
most characteristic rhythm disturbance of toxic digoxin levels
PAT (paroxysmal atrial tachycardia)
drugs that put pt at risk for V. tach and torsades
anti-arrhythmics, TCA, phenothiazines, erythromycin
effect of quinidine
prolonged QT interval
-also widened QRS
when should you d/c quinidine
QTI >25% prolongation
where do you seen osborne waves
hypothermia
all intervals with hypothermia are _____ (prolonged or shortened)
prolonged
what is an osborne wave
ST segment elevation with an abrupt ascent at the J point, then plunge back to baseline
most common arrhythmias a/w hypothermia
sinus bradycardia and slow a fib
what is brugade syndrome
EKG abnormalities which cause sudden death due to V. fib
-3 different EKG patterns with variable ST segment elevation abnl.
treatment for brugade syndrome
ICD (implantable cardioverter-defibrillator)
