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Cardiac Dysrhythmias and Interventions (part 2) - Med Surg Exam 3 (1)
Cardiac Dysrhythmias and Interventions (part 2) - Med Surg Exam 3 (1)
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Cardiac Dysrhythmias and Interventions(part 2) - Med Surg Exam 3
-prolonged AV conduction
-ECG: PR interval >0.20 seconds
-causes: ischemia, drug toxicity (dig., BB, CBB, flecainide), hypokalemia
-assessment: asymptomatic
-treatment: dig level, K+ level, monitor for lengthening (further block) - ANS-first-degree
av block
-progression of time it takes for impulse to get from SA to AV node until one doesn't get
through at all
-ECG: gradual lengthening of the PR interval -> nonconducted atrial impulse (blocked
ventricular beat)
-causes: drugs (dig., BB, CBB), ischemia/infarct
-assessment: transient and asymptomatic; monitor for further heart block, symptomatic
bradycardia
-treatment: atropine (symptomatic), temporary pacer (post MI)
-longer, longer, longer, drop; you know you have wenckebach) - ANS-second-degree AV
block type 1 (mobitz 1 or wenckebach)
-SA fires regularly, only some impulses are sent through
-ECG: regular R-R, constant PR interval, nonconducted P waves
-measured by ratio of success - 2:1, 3:1, variable
-causes: irritable AV node from ischemia/injury drug toxicity
-assessment: depends on ventricular rate (# of impulses sent through); often
progresses to 3rd degree - poor prognosis; decreased CO
-treatment: pacemaker; atropine NOT effective - ANS-second-degree AV block type 2
-disconnect between atria and ventricles (AV dissociation)
-ECG: atria and ventricles contract independently (no relationship between p wave and
QRS complex)
-causes: CAD, drug toxicity (dead/injured AV node)
-assessment: decreased CO -> ischemia/HF/shock, syncope
-treatment: need to pace! dopamine and epinephrine to increase HR and support BP -
ANS-third-degree AV block (complete heart block)
-If the R is far from the P then you have a first degree
, -Longer, longer, longer drop then you have a Wenckebach
-if some Ps don't get through then you have a second degree type II
-If Ps and Qs don't agree then you have a third degree - ANS-heart block poem
-early contraction from an ectopic focus in the ventricles
-ECG: wide, distorted, early QRS complex with compensatory pause
- - unifocal: rises from 1 location
- - bigeminy/trigeminy: occurs every 2nd or 3rd beat
- - couplet: 2 consecutive PVCs
- - ventricular tachycardia: 3 or more PVCs in a row
- - R on T phenomenon: PVC strikes on T wave (repolarization) induces ventricular
tachycardia or ventricular fibrillation
-causes: ischemia, stimulants, electrolyte imbalance, hypoxia, stress (clinical
significance depends on frequency)
-assessment: hemodynamic status, pulse (PVCs don't perfuse (no atrial contraction =
no blood in ventricle))
-treatment: oxygen, electrolyte replacement, BB, procainamide - if resistant to other
therapy (treat the cause) - ANS-premature ventricular contraction (PVC)
-irritable spot in ventricle takes over with rapid fire
-ECG: V: 150-250 bpm, buried P wave, wide and distorted QRS complex (>0.12)
- - run/nonsustained: NSVT (<30 secs)
- - sustained: >30 secs
- - monomorphic vs polymorphic (torsades de pointes)
-causes: MI, electrolyte imbalance, long QT syndrome, drug toxicity
-assessment: pulse (stable) or pulseless (unstable) - prepare for code
-treatment: VT requires CPR with defibrillation (pulseless); mag sulfate, IV lidocaine,
procainamide, sotalol, amiodarone - ANS-ventricular tachycardia
-multiple, irritable spots fire rapidly from the ventricles
- - 0 CO, lethal dysrhythmia
-ECG: course or fine ventricular quivering
-causes: ischemia, procedural catheter stimulation, coronary reperfusion, shocking on T
wave, hyperkalemia, hypoxemia, drug toxicity
-treatment: CPR, defibrillate, IV lidocaine, pronestyl, electrolyte replacement -
ANS-ventricular fibrillation
-absence of electrical activity
-ECG: flatline
-causes: CAD, severe conduction disturbance, end stage HF, prolonged arrest
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