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105 Cards in this Set

  • Front
  • Back
What is a cardiac arrhythmia?
A disturbance in the cardiac rhythm, which may or may not be significant.
one of the most important tasks in the pre hospital care of a pt with a ami is ?
Anticpate recongize and treat life threatning arrhythmias.
Very slow HRs lead to?
inadequate CO and often precede electrical instability of the heart
Conversly very rapid HRs
increase the work of the heart, causing further myocardial ishemia and damage
when is ekg analyis indicated
any patient who might have a cardia c related condition, any pt with a chest pain, should also be instituted for any pt with a history of heart problems, age is a contributing factor
a straight line ekg in an alert, comnunitve pt indicates what>
loose or disconnected lead, not aystole
wavy baseline resembling vfib may be caused by ?
pt movment or muscle tremor, check pt before getting pads or paddles to shock
what are bipolar leads?
limb leads, consist of two electrodes, one positive one negative place on two different limbs
what does a lead do?
offers electrical snap shot of certain parts of the heart
when using bipolar leads any impulse in the body moving t oa positive electrode will casue what?
positve deflection in ekg
conversly any impulse moving towards a negative electrode will cause what?
negative deflection in ekg
if impulse moves perpendicualtr to the lead the result will be ?
a biphasic waveform which is above and below the isoelectric baseline
most reliable way of analyzing a rhythm strip
use a systematic approach and examine every strip the same way
p wave normally?
upright wave form in leads I and II, alos immediatly preceds the QRS,
P wave is formed by the impulse generated where
sa node in the right atrium and spreads over the atria causing depolarization lasting 0.6- .011
what is the pr interval?
usually .12-.20 (three to 5 small boxes)
includes atrial deplorization and the conduction of the impulse through the av junction and the slight delay when the impulse is held in the av junction allowing time for ventricular filling
what is the QRS complex?
consist of three waveforms,represents deploraization, of two simultaneoulsy contracting ventricles
in healthy people the QRS complex is
narrow and with sharply pinted waves and shas duration of less than 0.12 usually .04 to0.11
normal QRS represents what?
conduction of the impulse has proceeded normally from the av junction throught the bubndle of his and the purkinje fibers
first downward delfection in QRS IS
q wave and represents conduction throught ventricular septum
first upward deflection is
the r wave most of both venticles are depolarixzed during r wave
any downward deflection after the rwave
second upward deflection
r prime wave and are never normal and they indicate troube in the conduction system of the ventricle
define j point
where the QRS complex ends and st segment begins, this it represents the end of depolarixation and the apparent of begining of repolarzation
st segment
line between the qrs complex and the beginning of the t wave is normally isolectric
st segment this significantly imm or one small box above or below the isolelectic line is highly suggestive of
myocardical ishemia or injury althogh a full 12 lead is required to determin the precise significance of the st segment elevation or depression
t wave
represents ventiriclar reploarization but may also show abnormalities such as those found with electrolyte disturbaces
what does a tall pwave and shrply preaked indicate?
QT interval
includes all activity that occurs during the qrs complex and t wave (ven depolorazation and repolarization) begins at ends with the t wave as it comes back to the isoelectric line if no q wave , measurments begin with the rwave
noramlly last .36 to .44
prolonged qt indactes the the heart is experancing
a extened refractory period, making the ventricle more vulnerable to arrhythmais may occur with administration of some drugs hypocalcemia an ami or pericarditis conversly a aa shortened at may indiacet hypercalcemia and pts on digitalis
Wandering atrial pacemaker is most commonly seen in pts with
significant lung disease, tx is usually not indiacted in the prehospital setting
existence of a particular comples with in another yhythm are aslo sknown as ectopic comploees meaning the occour out of normal location p waves is present and pright and precedes each qrs however its shpae differs from the sahpaes of the pwaves from the sa node
a tachy rhythm origination from the pace maker above the ventricles, occours when the tru orgin of a tachy is unknow a rhythm of atleast excedding 150 bpm
svt reflecting its tendacy to start and stop abrubtly, paroxysmal means occurring in spasms, you must witness it to call it psvt most up to dat trminlogy is reentry svt
rate of more than 100 in effect a tachycardic wandering atrial pacemaker mostly seen in pts with lung dieases
a flutter
a rhythm which the atria contract at a rate much too papid for the venticles to match the waves know as fwaves not p waves have a sawtooth shape
a fib
rhythm where the atria no longer contract but fibrillate or qui ver with out any organixed contraction usually no visiable pwaves irregularly irregular fairly common among elderly pts blood moving thru the fibirlating atria has tendacy to form small clots many elderly pts whose normal rhythm is afib tan ane anticoagulant med suach as warfain coumadin as wwe as digitalis to regualte the rate of ventricular response
junctional rhythm
occours when the sa node ceases function and the av node takes over as the pacemaker 40-60 bpm usually regualar p wave is inverted if visiable most commonly seen in pts with significant problems with the sa node little can be don in the field but pacing
accelerated junctional rhythm
60bpm remains less than 100 also regular seldom require tx in field, rate is usually fast enought to maintain a resonable co
rate depends on underlying rhythm, p wave if present will be inverted rarley tx in field
heart blocks
impulses traveling throught the av node are delayed more than usual
1st degree hb
hb pri greater than .20 rhythm is regular the only diff between normal sinus rhythm is the prolonged pri rarley tx in field
2nd degree type1 wenckebach
occours when an impulse reaching the av node is accasionally prevented from procceding to ventricles and causing a complex( when each impulse is delayed a little longer till finally one impulse is not allowed to continue
2nd degree type 2 mobitz 2 (classical)
occours when several impulses are not allowed to continue sometimes called classical the pri is always constant they are tx in feild if occours with brady that results in significantly dimished co
3rd hb complete
occurs when all impulses reaching the av node are prevented from procedding to the ventricles and causing a qrs complex because all impules from atria are blocked rhe venticles will delvelop there own pacemaker to continue circulation of blood rhythm is usually reg with p-p and r-r being constant pri is nonexstitant atrial rate of 60 -100 but ventricle rate being less than 60 tx in field if rate is brady and co is greatly diminished in such cases pt will require tcp
rhythms of the venticles
sa node fails av node fails the venticles may begin to originate their own impulses and become the pacemaker of the heart such rhythms will have missing p waves and wide qrs complexes
idioventricualr rhythm
has a rate of 20-40 bpm ido ryhthm usually reg p waves absent due to failure of sa and av node, the qrs complesx will measurer greater than 0.12 because it originates inthe venticles tx is geared toward improving co
accelerated idoventricular
exceeds its nmormal upper rate of 40 but remains less than 100 also considered reg seldom tx in feild
occour when the sa and av nodes fails as the pacemakers of the heart any rhythm that results in a ventricualr rate greater than 100 bpm is considerd tachy vtach is regular,
monomorphic vtach
having one common shape of qrs complex
polymorphic vtach
qrs complexes that vary in height in an alternating pattern t
torsade de pointes
most common polymorphic vtach usually seen in pts who have a conditon of a prolonged q0t interval may be normal for pts or it may be induced by meds or drugs such as quinidine usually considered worse than mono vtach and converts spontaneoulsyt back to a normal rhythm or degernates into vfib
tx of vtach
serious condition rate usually too fast to main tain adequate co usually leasds to ventricular failure or vifib
most commonly origiante from ishemia in the ventricular tissue they generally considered more serius than pac or pjc. Multifocal couplet an bigmjeiny pvc are considered more serious than unifocal pvc
hazard of pvc
they might occour when the ventricles are not fully repolarized as indicated by the twave so called ron t phenomnon often reults in vfib not usually tx in field unless co is greatly affecting and m ucst be treated with caution
rhythm in which the entire heart is no longer contracting but rather fibrilllating or quivering without any oraganized contraction random cell depolorazation rather than from the sa node impulse no pwaves no ars no pri
most commonly seen in adults who go into cardiac arrest responds well to defib
flat line which the entier heart is no longer contracting but rather sitting still within the thorax complete absencse of electrical impulses in heart occurs when many cell of the heart have been hypoxic for so long they no longer have energy for contraction
artificial pacemaker
firing artificial pacemaker causes a uniquie vertical spike on the ekg tracing you attach a pt and see sharp verical spikes on the ekg
common type is
ventricular pacemaker attached to the ventricles only causes shapr pacemaker spike followed by a wide qrs
atria and vnticle
attached to both produces spike followed by pwave and another spike followed by qrs
demand pacemaker
newer pacemakers equipped with snsors that can identify the rate of spontanwous depolariztion of the heart these usually gerate pacing impulses only when they sense that the natural pace of cardiac impulses has slowed below a specific number usualyy 60
if pacemaker is failing
the spikes may still be visiable but will not be followed by qrs ( loss of capture) battery failure or if wires become lose pts need tcp as quickly as possiable
runaway pacemaker
very tachy pacemaker rhythm that mush bye slowed to preserve the pts cardiac function, usually a strong magnet placed over site will reset it
delta wave is a indiacation of what
wolff parkinson white (WPW) syndrome pts have a accessory pathway between the atria and the ventricles called the bundle of kent
aberrant conduction
budle of kent confuctive tissue bypasses the av node and begins ventricualr depolarixation early resulting in a prapid up slope to the r wave immediatetly after the end of the p wave can be seen as a widend qrs complex more than 0.12 wheich woulod seem to indicate a ventricular pacemaker pts with wpw are suseptible to svts
osborne or jwave
occurs in cases of hyopthermia and presents as what apperas to be a pwave ath the end o the qrs complex generally the more serious the hypothermia the larger the jwave should be considered only as indication of hypothermia
2 electrolyte imbalances that cause changes in ekg 2 most common
hyperkalemia presents with very tall poited t waves
hypokalemia presents with flat or appareently absent twaves and development of u waves smaller even than a pwave that occurs after a twave but before the next pwave very uncommon and mistaken for extra peaves
other electrolyte imbalances do not cause obvious changes in ekg
hypercalcemia may cause a shortened qti
hypoclacemia may slightly lenghtne the qti likley not be obvious in field
purpose of 12 lead ekg
to localize injury to heart muscle however we must be able to look at the heart from several angles
provides electrical picture of the heart taken from a specified vantage point
12 leads
12 different pictures of the heart
limb leads
I, II, III, aVR aVL aVF these leads are are derived from attaching cables to the pts limbs look at the heart from the sides and from the feet in the vertical plane
pericordial leads
v1 to v6 also chest leads anterior leads or v leads placed on the anterior and lateral chest wasll look at the heart in a horzontal plane front(anterior wall of heart) and from the ledft side anterolateral v1 v2 look at septum v3 and v4 look at the anteror wall of the left ventricle and v5 anv6 look at the lateral wall of the left ventrical
the left ventricle
is tyhe stronger and more muscular of the two ventricles it will be the first to let its owner know that it is not getting enouhg oxygen if becomes damaged in addition to pain pt may develop deadly arrhythimais such as vfib
each wall requires 2 to 4 leads
or views to see its image completely these leads are anatomically contigous
leads look at the same general area of the heart ( when we are looking for evidence of injury to the heart we must see it in 2 or more contiguous leads
contiguous inferior leads
contiguous septal anterior lateral leads
v6-lead 1
evidence pt is having an ami we must focus on three parts of the ekg
the st segment the q wave and the t wave
sequence of a ami
blood supply to the affected area of the hearmuscle slows to a trickle the muscle no longer receives sufficient o2 this it becomes ishemic (deprived of blood) if ischemia persist mote than a few minutes it leads to actual injurt to the hear muscle which in turn will be followeed by infarction (death of muscle) if cirulation to the area is not rpidly restored
ischemia commonly causes
st depression and may lead to t wave inversion
injury will cause
st segment elevation if left untreated it will lead to infarction
infarction often leads to what kind of wave
pathological q wave a q wace that is wider than 0.04 or deeper than on third of the height of the r wave that follows it and is seen in two or more contigous leads generally indicates a infarction has happened in the past
40% of pts experince an inferior wall mi
a right ventricular mi will eventually develop as well
how can you verify right ventricular mi ?
an electrode placed in the fifth intercostal space at the midclavicular line on the right side of the chest V4R TAKE THE V4 ON THE LEFT AND PUT IT ON THE RIGHT IF YOU SEE ST SEGMENT ELEVATION of greater than 1mm in the v4r lead there is a high likelihood that you have identified a right ventricular mi
why not given pts with a right ventricle mi nitro?c
they may already be hypotensive or become hypotensive if nitro is given you may be ordered to give 1-2 l of saline before nitro is given
the absence of a mi on ekg means?
doesnt meant the pt isnt having one
time is ?
myocardium (muscle)
"code" or
CarDiOpulmonary arrEst
Cardiac arrest victims usually have evidence of atherosclerosis or other underlying cardiac disesase however can also occur aftyer
electrocution drowning and other trpes of trauma
universal algorithm (bls healthcare provider algorithm)
assess responsiveness Open airway look list4en and feel for breathing not breathering give two slow breathes
2 asess the circulation no pulse start cpr attach monitor defib
if patients in cardiac arrest he or sh may be in any of the following rhythms
vfib or pulesless vtach
pea aystole
vfib or pulseless vtach is probably the most important pathway down the algorithm for you to follow why?
because pts in these are the most likely to be successfully resuscitated if they reciece timely and appropiate tx
vfib and pulseless vtach management
1 check abc as described in bls algorithm
2 perform cpr 2 mins while defib is being put on
3 confirm rhythm vfib vtach
4confirm absense of pulse max 10 seconds
5 resume cpr while charging defib
6 clear pt and defib
defib at 200j if biphasic and
360 if monophasic
7 resume cpr at end of discharge 2mins cpr then stop and reassess the pts cirulation and rhythm
8 if rhythm other than vtach of vfib appears on the monitor identify new rhythm if there is no pulse move to asystole pea path way and RESUME CPR IMMEDIATLY if there is a pulse move to appropiate algo for it if rhythm is persistant vfib or vtach resume cpr while charging defib
9 shock again
10 resume cpr again for 2mins
11 during this cpr a advanced airway should be inserted verify placement with mulitple methods once pt been intubated no need to stop compressions for ventialtions
12 start iv with normal saline iv/io
13 adminster a vassopressor drug epi or vassopessin follow immeditely with 20 to 30 ml of bolus iv fluid and elevate the extremity to facilitate delivery
14 end of 2mins of cpr check for circulation and check the rhythm on moitor
15 if vfib or vtach resume cpr while charging defib
16 clear pt and shock
17 resume cpr immediately 2 mins during this 2 mins you should consider antiarrhythmics meds amiodorne or lidocaine
18 end of 2mins check for circulation and check monitor for rhythm
19 vfib or vtach still present resume cpr while charging the defib
20 clear pt and shock
21 resume cpr immediatley
22 if vfib vtach still prsent consider making a transport decision whith adivse from med control continue the cycle of dfib while adminstering repeared doses of meds
if at any time during this sequence the is retrun of circulation asses pts vitals support airway povide meds as indicated for regulating the hr
epi given for vfib vtach 1st line
vassopressin 1st line
amiodarone 2line
lidocaine 2line
1mg every 3-5mins
40 units iv push one time only vassopressin can be given in place of the first or second dose of epi but not both
amio- 300mg bolus may be repeated once at 150mg in 3-5mins after initial dose
lido-1-1.5 can be repeated at 0.5 to 0.75 untill max dose of 3mg/kg is reached
tx for PEA
when monitor is applied to pulseless pt and rhythm other than vtach or vfib is seen:
1 resume cpr
2 insert advanced airway
3 start iv normal saline iv/io
4 adminster vassopressor drug
5 at end of 2mins cpr check for circulation and check for the rhythm
6 if pea still present continbue cpr
search for and treat possiable causes
if pea occurs in the context of bradycardia give atropine if rate on monitor is 60 or higher in pea atropine is not indicated
drugs for pea tx
atropine if occours in context of bradycardia
epi- 1mg iv push repeated every 3-5mins for aslong as pulse is absent
vassopressin- 40 unts iv push one time only can be given in place of epi firs or second dose but not both
atropine brady 1mg iv may be repeated 3-5mins to a total dose of 0.04 mg/kg
h and t
hypovolemia - volume infusion
hypoxemia - intubation 100%02
hpoglycemia-D50 in water 25 g
hyperkalamia -immediate transport
hydrogen ions- sodium bicarb if certian of acidosis
tension pneumothorax needle decompression
cardiac tamponade immeditate transport
others (drug overdoses narcan for drug overdoses) trauma massive mi pulmonary embolism) immediate transport
postresuscitative care
1 stablize cardiac rhythm give an antiarrhymic drug for vtach vfib give atropine or pacing for symptomatic brady
2 normalize the bp give dopemine or norepi infusion ot raise the systolic bp to 100 mm Hg
2 elevate pts head to 30 if the bp allows
management of symptomatic bradycardia
pt who present with or develops symptomatic brady needs to be treated in a manner that wil lincrease the hr and improve co a altered metal status and hypotension are common indications for tx assumming that airway and breathring have been suppo0rted
1 establish iv
2 atropine 0.5mg bolus may repeat every 3to5 mins until hr is normal or max dose of 0.04 mg/kg
3 if pt is severly compromise or doesent respond to atropine establish tcp as quickly as possiable if pt in second type 2 or third degree hb tcp is the fist line tx
4 if atropine or tcp are unaffective considedr sympathomimetic drug most commonly dopemine 2-10 mcg /kg/min milder or epi drip rate of 2-10mcgmin mix 1mg of epi in into 250 ml bg of ns drip rate of 30 drops a min with microdrip admin
5 transport
stimulation of vagal nerve
stimulates the parasympathetic nervous system to slow the heart
tachy with pulse
1 abc give o2 monitor ekg bp oximetry
idenitfy and treat reversialbe causes
2 pt stable ? unstable includes altered metal status ongoing chest pain hypotension or other signs of shock
if unstable perform sychornized cardioversion establish iv access give sedation if pt is conscous
5 stable estabilsh iv obtain 12 lead ekg is qrs narrow or wide ?
narrow qrs reg
attempt vagal
give adenosine 6mg rapid if no conversion give 12 mg rapid may repeat 12 mg once
dose rythm convert? IF YES PROBALE REENTRY SVT treat reoccourance with adenosine or longer acting av nodal blocking agents dilitazem beta blockers i
IF RHYTHM does not convert possiable atrial flutter ectopic atrial tach or juctional tach control rate ie dilitiazem beta blockers treat underlying cause
wide qrs rhythm reg or irreg
reg if vntricular tack or uncertain give amioadrone 150 mg iv over 10 min repeat as needed to max dose of 2.2g-24hours prepare for elective cardioversion if svt give adensoin
IF IRREG ATRIAL FIB control rate consider expert consulation
contol rate dilitazem beta blockers
if pre excited atiral fib af plus wpw avoid av nodal blockers adenosine digoxin dlitiaxem verpamil consdier antiarrythmics amio 150mg iv over 10 minutes if recurrent plooymorphic vt seek expert
if torsade de pointes give magnesuium 1-2 grams over 5-60 mins then infusion