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bility of cell to respond to stimulus
ability of cell to reach threshold potential and generate impulses without an outside stimulus
SA node is:
- pacemaker of the heart
- sets pace and transmits impulses throughout the myocardium
ability of the muscle to move an impulse from cell to cell
what neurotransmitters work within the sympathetic (adrenergic) nervous system?
what do epi and norepi do in the body?
- raise BP
- increase HR
- enhance force of myocardial contraction
which NT works with cholinergic parasympathetic nervous system?
- --decrease HR
- --lower BP
- --reduce force of myocardial contraction
rate of Bundle of His?
rate of bundle branches?
- purkinjie fibers? 15-40
during resting state what levels are these electrolytes at INSIDE cell?
- Na+ lower
- K+ higher
- Ca+ lower
what happens to K+, Na+, and Ca++ during depolarization in reference to cells?
- heart contracts due to Na+ and Ca+ moving into cell
- and K+ moves out
what is action potential?
return to resting state
what is EKG?
graphic display of conduction
monophasic action potential?
depolarization and repolarization of cardiac muscle cells
what are dysrythmias?
- disorders of the hearts conduction
- disturbance in rate, rhythm or both
- ID by analyzing EKG
- ventricular depolarization
- contraction of the ventricles
- atrial depolarization
- contraction of the atrium
duration of P wave should be:
less than 3 small squares OR <.11
normal PR interval?
- indicates AV conduction time
steps for interpretation of EKG?
- 1. look for P-QRS-T
- 2. determine rate..atrial= count P waves, ventricular= count R waves
- 3. determine A-V rhythms, R-R for regularity
minor regular variations in HR and pulse pressure assoc with resp
- <60 BPM, left untreated if asymptomatic
- Symptomatic: Atropine IV, Dopamine, Epi
- >100 BPM
- caused by fever, etc
Tx for atrial flutter?
- anticoagulation, Cardizem, Digoxin
- if unstable: cardioversion
- caused by: aging, hypoxia, electrolyte disturbances, increased atrial pressures, tricuspid vavle disease
- saw-tooth shaped waves, 200-350 threat of clotting
Tx for A fib?
- Goal: to decrease atrial irritation, decrease rate of ventricular response
- CHRONIC: anticoagulation, Warfarin (coumadin), Digoxin, Cardizem, cardioversion if meds not effective synchronized
- threat of clotting
so pt doesnt go into vfib and need defibrillation
First degree heart block?
- PR = >.20 (prolonged)
- delayed conduction through the AV junction
- Amiodarone bolus 150 mg over 10 mins
- IV flow of 1 mg/minute
- may need oral antiarrythmic
Cardioversion and defib are synchronized or not?
- cardioversion- synchronized
- defibrillation- unsynchronized
- most commonly following termination of atrial, AV junctional or ventricular tachycardias. this pause is usually insignificant
- in AMI, CAD asystole may continue: cardiac arrest
- Tx: CPR, artificial pacing, Epi, atropine
complications of pacemakers use?
- bleeding, hematoma
- dislocation of lead
- cardiac tampponade
- pacemaker malfunction
sympathetic system: fight or flight:
increase HR, and BP, enhance force of contractions
during resting state, K+ is where?
V Tach Tx?
- 1. epi
- 2. amiodarone
- 3. lidocaine
- 4. procainamide
V fib tx?
- epi 1 mg
- vasopressin 40 U
AV node pacemaker, what type of rhythm is there?
- Junctional- absent or inverted P wave
- 40-60 bpm
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