Transcript Stable (narrow QRS complex)

“EKG” electrocardiogram
Gail L. Lupica PhD, RN, CNE
Nurs 211
“EKG”
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Take your pulse.
What you feel is blood rushing through your
radial artery with each systolic contraction.
Systole creates that push of blood. Diastole
allows the chambers to fill again. That is what’s
happening to our heart mechanically.
What fuels this machine???
“EKG”
Electricity fuels this machine!
 A spot right above our atrium called the
Sinoatrial node has “automaticity”,
which means it fires without any other
assistance.
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“EKG”
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The SA node fires. The impulse travels through
the internodal tracts to the AV node.
From there it travels to the bundle of his then
down the right and left bundles.
The purkinje fibers conduct the impulse rapidly
through the muscle until it “depolarizes”
The depolarization causes our muscles to
contract and that’s what pushes the blood
through our arteries.
“EKG”
When our patients are in the hospital we
not only want to HEAR, and FEEL the
heart, we want to SEE how normal the
electricity is that’s causing it to pump.
 We can find that information on an
electrocardiogram.
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“EKG”
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We need to use special paper to
understand that report completely. That
paper looks like this>>>
“EKG”
Each teeny tiny box represents .04
seconds.
 Adding up the teeny tiny boxes across the
paper lets you know how long it took for
the current to travel.
 5 boxes = ?? seconds
 .04 x 5 = .20 seconds
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“EKG”- “normal”
Certain pictures or rhythms that we get are
considered “normal”.
 We call these rhythms “normal sinus
rhythm”
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Normal…..
Sinus…….. Rhythm
(no problems) (from SA node) (pattern)
“EKG” - p wave, qrs complex
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The p-wave represents atrial
depolarization. The electricity started in the
SA node, traveled to the AV node. The p wave
bump shows you that the atria contracted. (the
filling of the ventricles prior to systolic
contraction) The distance between the beginning
of the p-wave and the beginning of the QRS
interval is the P-R interval.
The QRS complex represents ventricular
depolarization
Components of a normal electrocardiogram
Elsevier items and derived items © 2006 by Elsevier Inc.
April 17
14
“EKG” criteria for normal sinus rhythm.
To judge what’s normal, you have to understand
“normal”. Certain criteria for EKGs meet the
criteria for normal sinus rhythm.
The distance between the beginning of the p wave to the beginning of
the QRS complex needs to be less that .20 seconds, or 5 teeny boxes
(= 1 bigger box).
 Each QRS complex needs to be less than .12 seconds or 3 teeny
boxes.
EKG - criteria for normal sinus rhythm.
The QRS complexes need to be equal distant apart.
 Each P wave should be followed by a QRS complex.
 You should have no more than 10 complexes in a 6 second
strip and no LESS than 6. (HR 60-100)
 The t waves should look upright and round (& stay away
from them during defibrillation!!!!!!)
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“EKG” Rate determination
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15 LARGE boxes is 3 seconds, 30 LARGE
boxes is 6 seconds. Count the number of
complexes in a 6 sec strip and multiply by 10.
Count the number of small boxes between 2
QRS complexes and divide that number into
1500. Ex: 1500/15 = 100bpm
Big block method-300, 150, 100, 75….
NOW, Let’s Practice
Rate- 6 second interval x 10
Rate: 30 blocks is 6 secs x 10
Rate:1500 method: 1500/4 = 75
Let’s go onto look at:
Sinus bradycardia
 Sinus tacycardia
 Atrial fibrillation
 Atrial flutter
 Premature ventricular contractions
 Ventricular tachycardia
 Ventricular fibrillation
 Asysytole
& HOW TO TREAT THEM!!!
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What’s this?
Why?
BradycardiaWhat’s more important, a patient’s heart
rate or the patient signs of perfusion and
hemodynamic sufficiency?
 Absolute bradycardia- HR <60
 Relative bradycardia- Pt is showing signs
of inadequate CO even with a HR> 60.
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Sinus Bradycardia-treat
Atropine: The first drug of choice for
symptomatic bradycardia.
 0.5mg IV push and may repeat up to a
total dose of 3mg.
 anticholinergic drug and increases firing of
the SA Node by blocking the action of the
vagas nerve on the heart resulting in an
increased heart rate.
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Sinus Bradycardia-treat
Dopamine: Second-line drug for
symptomatic bradycardia when atropine is
not effective.
2-10 micrograms/kg/min infusion.
• Epinephrine: equal alternative to
dopamine. : 1mg epinephrine is mixed with
500ml of NS or D5W—
• 2-10 micrograms/min (titrated to effect).
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Sinus Brady-TCP
Transcutaneous pacing (TCP)should be taking place as atropine is being
given.
 If atropine fails, TCP should be initiated.
 For the patient with signs of poor
perfusion, transcutaneous pacing is the
treatment of choice.
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What’s this?
Why?
Sinus Tachycardia- (vs SVT)
Dehydration??, hypoxia??, fever??,
and sepsis??.
 …H’s and T’s
 Administration of OXYGEN and
NORMAL SALINE are of primary
importance for the treatment of causative
factors …..
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Sinus Tachycardia- (vs SVT)
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SVT- Treat the underlying Cause!!
(5 Hs and 5 Ts)
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The H’s:Hypovolemia, Hypoxia, Hydrogen
ion (acidosis), Hyper/hypokalemia,Hypoglycemia,Hypothermia.
TheT’sinclude:Toxins,Tamponade(cardia),
Tension pneumothorax, Thrombosis
(coronary and pulmonary), and Trauma.
ST vs SVT- treat
With SVT, impulses in the atria fire
rapidly and cause interference with
the SA node.
 But in sinus tachycardia, the heart is
functioning normally; only the SA node is
firing at a higher than normal rate. Also
SVTs can originate from several different
spots within the atria.
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Sinus Tachycardia vs SVT
> 120
 Stable vs unstable
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Unstable?
Synchronized
cardioversion
ST SVT- treat
Synchronized
cardioversion vs
defibrillation- What’s
the difference?
Sinus Tachycardia vs SVT-treat
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Stable??
Stable (narrow QRS complex) → vagal
maneuvers → adenosine (if regular) →
beta-blocker/calcium channel
blocker → get an expert
Stable (wide) → adenosine → consider
antiarrhythmic infusion → get an expert
Sinus tachy vs. SVT- adenosine
Used when vagal maneuvers fail
 slows cardiac conduction through the AV
node. Interrupts reentry (SVT causing)
pathways through the AV node
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St-SVT- adenosine
6 mg administered rapidly over 1-3
seconds followed by a 20 ml NS bolus.
 does not convert out of SVT within 1 to 2
minutes, a second 12 mg dose may
be given in similar fashion.
 Administer adenosine as quickly
as possible.
 side effects -flushing, chest pain/tightness,
brief asystole or bradycardia.
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What’s this?
Why?
Atrial Fibrillation –treat
Unstable?- synchronized cardioversion
 What are you worried about with this
dysrhythmia?
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 1.
 2.
Atrial fibrillation
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Animations
 Cardioversion
 Diltiazem
 Heparin
What’s this?
Why?
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Why?
Ventricular dysrhythmiasPVCs- Amiodarone
Cordarone
 Antiarrhythmic
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1. •Increases
the action potential duration
2. Increases the refractory period in the atria,
ventricles and AV node
PVCs- Amiodarone- dosing
150 mg IV bolus over10 minutes at 15
mg/min.
 Maintenance infusion of 1 mg/min for 6
hours,
 then slowly reducing to 0.5 mg/min over
the next 18 hours.
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What’s this?
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Ventricular Tachycardia-Ventricular
fibrillation- treat-defib
CPR 2min/5 cycles
 Biphasic (the electrical current travels from
one paddle to the other paddle and then
back). 120-200 Joules to shock.
 Then what?
 Shock , drug, shock, drug
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Ventricular Tachycardia-Ventricular
fibrillation- treat-defib
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epi?
Epi
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Intravenous Push/IO: 1mg epinephrine IV
is given every 3-5 minutes.
Endotracheal Tube: 2-2.5mg epinephrine
is diluted in 10cc NS and given directly
into the ET tube.
Amiodarone
(Pulseless VT of VF): Initial bolus of 300
mg IV diluted in 20 - 30 ml of NS or D5W.
repeat doses of 150 mg IV every 3 - 5
minutes. …1 mg/min infusion for 6 hours,
then reduce 0.5 mg/min for the next 18
hours
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