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213 Exam 1-ONeal

213 Exam 1 - O'Neal

after you exercise what happens to your o2 demand it increases
does an increase in your demand increase your o2 supply yes
in what way does your body compensate for an increase in o2 supply and demand it increases your HR
what is it called - how much blood volume is going out per stroke stroke volume
does your stroke volume change during little exercise no - just your HR increases
with a hr of up to about 132 bpm your heart has enough time to fill with the same volume (amnt of blood)
what is the formula for cardiac output HR x Stroke volume
what is the blood flow thru the heart superior & inferior cava-rt atrium-tricuspid valve-rt ventricle-pulmonic valve (now it goes into the pulmonary system)-pulmonary artery-pulmonary veins-L atrium-mitral valve-L ventricle-aortic valve-to body
what is the o2 content of the pulmonary artery zero because its come from the body - the venous side and hasn't had time to re-o2 yet.
which ventricle is larger and why the Left one - it pumps blood to the body and the body's pressure is more than the pulmonary pressure
which ventricle would use up more 02-one with 150 pressure or one with 120 120
what is a normal diastolic pressure in the ventricle 6-12
what happens during diastole in the ventricle the coronary artery will fill
diastole is when the ventricle relaxes so that it can fill
what is cardiac output approx 4-8 L/min
example is Jared and June-Jared is bigger than June and they both have a cardiac output of around 4-who is better perfussed June-because she has less body to perfuse.
what is cardiac index the amnt of perfusion per body service area
what is a normal cardiac index 2.2 or higher
June probably had a higher cardiac index
% of total volume being ejected into the body ejection fraction
what is a normal ejection fraction 50-70%
4 determinants of cardiac output are HR-preload-afterload-contractility
some diagnostic ways to measure CO are PA catheter-clinical s/s (are they a&o-skin color normal-skin temp-mucus membranes pink-resp even deep and unlabored)
on a chest x-ray if you see black what is this air
what do you see on a chest xray if there is fluid white
if the pulmonary vasculature is congested what does this mean there is too much fluid (blood)
if you get to a point where you have too much fluid and it leaks out then what do you get pulmonary edema
what does BNP mean and where does it come from brain natriuetic peptide-the heart releases this - if the heart is failing the bnp is high
when are other situtions when BNP is high angina-hypotensive-MI-LV hypertrophy
if HR is up is CO up yes
if HR is up is CO down it could be if the person was severly tacchy
if HR is down is CO down yes
what is the 1st thing you should always find out first always find out what it is that is making the HR low or high. it could be meds or the person may be an athlete.
if a pts bp is in the 140's and you want to bring it down you could give a Ca chanel blocker or a beta blocker but what must you also know the pts BP as these meds also lower the Bp
you need to know WHAT CAUSED IT-it maybe meds or the pt may be an athlete
preload-what does preload reflect volume which reflects workload
the heart is the most full at the end of what diastole
so we want to know what is the preload when the heart is the most full (at the end of diastole) what is this called LVEDP - left ventricular end diastolic pressure
when does the heart have the highest pressure when it's the most full - (at the end of diastole)
an example of this is: in 1 class there were 30 people and in the other 60 people - which class caused the most workload the one with 60
so how can we measure the pressure in the left ventricle? - how would you get a catheter there have to go arterially against the blood flow-cross over the aortic valve then stick the catheter in.
what 2 pressures has research shown to be the same PA and LVEDP
so how do we get a PA catheter to sit in the PA go thru the right side of the heart thru the venous-cross over the tricuspid valve then the pulmonic valve and the catheter can sit right in the PA
what happens if the balloon floats thru into the pulmonary artery too much it will get wedged in the PA-that is called a wedge (PAWP)-this is the same pressure as a LVEDP
where is the tip of a central located superior vena cava right outside the rt atrium
what pressure can that get us CVP (it's closer to the rt side - venous side of the heart)
which side of the heart does a catheter tell us most about the side that it is closest to or the opposite side
which 2 pressures are more specific to the left side of the heart cap wedge or LVEDP
Initially which side of the heart fails the L side
usually the right side of the heart will fail because the l side has failed
what do diuretics get rid of pulmonary congestion
what happens to pressure as volume increases it increases
what happens to pressure as volume decreases it decreases
what is a normal LVEDP 6-12
what is a normal PAWP 6-12
what is a normal PA diastolic pressure 6-12
what is a normal CVP 4-6
why is the CVP pressure lower than the others because its the rt side of the heart and the rt side of the heart doesn't do as much work as the L side
why is a wedge not good for a pt because it can cut off o2 supply
what does too much pressure do to the heart it makes the heart back up
is there a correlation between L sided pressure and rt sided pressure? yes-if the L pressure goes up then the rt pressure goes up and vice versa
if someone has crackles mid way down in their lobes is their pressure 6-12 no its probably higher-they have more volume and because of the volume increase they have a pressure increase so it would be more than 6-12
what is the primary function of a pulmonary artery catheter to help evaluate L ventricular pressure/volume and function
if I have a big old floppy heart does it need more volume than a normal hear yes
what is a floppy heart called a sick heart
what is the EF usually for a sick heart <35
so what is the pressure like for a sick heart and why it's probably closer to 18 because they need more volume and the higher the volume the higher the pressure
what would someone probably be on as a standing order if they had a sick heart lasix-because they have more volume
what does Starlings law say the more the heart is filled during diastole the more forcefully it contracts like stretching a rubber band
Starlings law is right except when if you have a sick heart-because a sick heart is like an overstretched rubber band or stretched out underwear
increased volume results in what 3 things increased stretch, stroke volume, cardiac output
If our preload decreases then what happens to out volume it decreases
an increase in preload reflects an increase in volume unless overstretching - if overstretched you have a decreased CO and increased o2 consumption-why do you have an increase in 02 demand the heart is working harder
what are 4 things that decrease preload (volume) bleeding, diuresis, venous dilation(decreases flow coming into the heart) - arterial dilation
if you were giving a drug would you try to dilate the venous or arterial side venous-because
what are 3 drugs we give to diuresis lasix, diuril and bumex
what drugs vasodilate the venous system nitroglycerin
is there an actual change in the amnt of volume when preload is decreased by vasodilation no - it is just re-distributed
what is afterload its basically the force that is needed for the heart to eject the blood to the body
is afterload venous or arterial arterial
how is afterload measured SVR-systemic vascular resistance
what is a normal SVR number 800-1200
think of preload like a door opening and the room filling then think of afterload as the force it takes for the people to leave the room and push open the door
increased afterload = increase in forces opposing ventricular ejection
what does an increased afterload do to CO decreases it
T or F - increased afterload decreases cardiac output t
T or F - increased afterload makes the heart work harder T
T or F - increased afterload increases oxygen demand T-because the heart is working harder
T or F - increased afterload increases oxygen consumption T
can a heart that is ischemic due to coronary artery disease easily tolerate an increased afterload no-it needs more 02 because it is working harder and it can't get more o2 because it's ischemic
what happens if you are overworking your heart and it can't pump forward properly it backs up
to increase cardiac output what can we do to afterload decrease it
decreased afterload does what to 02 demand and consumption it decreases it
what does a decreased afterload do to cardiac output it increases it
what are 2 ways that we can decrease afterload decrease SVR or give arterial vasodilators
what are 4 arterial vasodilators ACE inhibitors, ARB's, Ca channel blockers and Nipride (Nipride is a very potent vasodilator given IV)
what is a venous dilator nitrates
increased contractility means what for CO increased
what are some ways we can increase contractility of the heart positive Ionotropes, beta adrenergic agonists, phosphodiesterase inhibitors
what do positive Ionotropes exactly do to the heart help it squeeze better
what is a positive Ionotropes Digoxin,
what are some s/s of digoxin toxicity anorexia, n/v, visual disturbances, (halo, yellow vision) arrithmias
what are 3 beta adrenergic agonists dopamine, dobutamine, epi
what 2 things do phosphodiesterase inhibitors do increase contractility and decrease afterload
why should we decrease contractility (2) it protects the heart by decreasing work load and decreases 02 consumption and demand
what drugs decrease contractility beta blockers
what are the 2 most common circulatory assist devices IABP (Intra aortic balloon pump and VAD-(ventricular assist device)
what 2 things does a IABP do decreases afterload and increases coronary perfusion (remember Youtube video)
when is a VAD used until the heart recovers or a donor is found
what are 3 drugs that decrease HR beta blockers, Ca chanel blockers, digoxin
what are 2 drugs that decrease preload diuretics and venous dilators such as ntg
what are 4 drugs that decrease afterload ACE inhibitors, ARBS, Arterial dilators like Nipride and Ca Chanel blockers
what are 2 types of drugs that increase contractility positive ionotropes and phosphodiesterase inhibitors
what are 4 positive ionotropes digoxin, dopamine, dobutamine, epinephrine
what are 2 phosphodiesterase inhibitors Inacor and Primacor
what 3 things to beta blockers do decrease HR, decrease BP and decrease contractility
what 4 things do Ca Chanel blockers do vasodilate (arterial)-Decrease BP-decrease HR-decrease afterload
what 3 things do ACE inhibitors do vasodilate (arterial)-decrease BP-decrease afterload
what 4 things do ARBs do block the action of angiotensin II- vasodilate (arterial)-decrease BP-decrease afterload
review coronary arteries - L, R, Left anterior descending and L circumflex
comes from an incomplete obstruction angina
comes from a complete obstruction infarction
across the wall of the heart muscle-it gets all layers of the heart transmural MI
just involves 1 layer of the heart subendocardial MI
which one is worst - transmural or subendocardial transmural
a MI will more than likely occur if there is ischemia to the heart for how long more than 20 minutes
it involves cell death and tissue necrosis
review name and location of MI's - anterior, inferior, lateral, septal
healing process of an MI - what are release in the first 24 hrs after an MI enzymes
what happens after 6 hrs physical changes
necrotic tissue removal happens how long after an MI 2-3 days
when is necrotic tissue replaced by scar 6 weeks after the MI
when is a thin walled firm scar formed 2-3 months
what is it called if it is dead, scarred, and cannot be helped infarction
what is it called if it is swollen, but can heal and must be protected injured
what is it when there is no permanent damage unless prolonged ischemic
angina pain or MI pain- substernal or elsewhere angina or MI
precipitated by stress or exertion angina
relieved by NTG or rest angina
lasts >30 mins MI
may occur without cause MI
pattern: stress, pain, rest, relief angina
usually not relieved MI
usually have associated symptoms MI
what are some of the associated symptoms n/v, epigastric pain, arrhythmias, s3 or s4, fever, crackles, jvd, decreased UO, fear, SOB, sweating
what are the 3 things that have to be present for an MI clinical presentations, serum cardiac markers, EKG changes
what are some of the cardiac markers seen after someone has a heart attack CK or CPK - CK MB bands - Toponin
which one is specific to cardiac muscle CK MB bands
which one is the MOST specific to cardiac muscle Troponin
when do ck levels rise in 3-12 hrs
when do CK levels peak in 24 hrs
when do CK levels go back to normal in 2-3 days
how do they draw the CK MB bands in a series of 3 - and drawn 6 hrs apart
**** NOTE to confirm a HA ALL 3 cardiac enzymes need to be elevated.
if CK is normal and MB is elevated has the pt had a HA no
when do we suspect a HA if MB and troponin are both elevated.
if there is an ST elevation what does this mean infarction
if there is an ST depression what does this mean ischemia
what does Q wave mean old infarction
what does MONA stand for morphine, oxygen, nitro, asprin
what are some other dx measures for an MI elevated WBC count, Thallium scan, blood glucose,
what are the emergency management things to do for someone with an MI ABC's, monitor EKG, establish IV access, RRT if needed, 12 lead EKG, v/s q 5 mins (this is how long it takes for nitro to take effect)
FACT-80-90% of MI's are secondary to a thrombus
what is the main goal to salvage as much muscle as possible
when is the only time we like to see arrhythmias when there has been immediate reprefussion
what are the 4 inclusions for thrombolytic therapy chest pain for less than 6 hours, intermittent chest pain, 12 lead EKG MI changes and PT is not predisposed to bleed
what are some drug therapies we could give to someone with an MI (6) IV Ntg-antiarrthymics-morphine-beta blockers-ace inhibitors asprin (81-325mg daily)
what 5 things does IV nitroglycerin do reduce pain-decreases preload-some decrease in afterload-increase in 02 supply and increases circulation to injured areas
what is the most common complication of a heart attack arrhythmias
what is the "King" of antiarrhythmia drugs Amiodorone
what is one other drug they use to treat arrhythmias lidocaine
do they usually treat arrhythmias no - only if they are sustained and life threatning
morphine is used to decrease anxiety also in the pt - it is also used to reduce cardiac workload-what are 3 ways it does this lowers consumption-reduces contractility-lowers bp and HR
what can morphine do to respirations depress them
what kind of drug is ASA an antiplatelet
what 3 things do beta blockers do when you are giving them with an MI decrease HR-decrease contractility-some decrease preload
what 2 things do ACE inhibitors/ARBS do decrease afterlaod-help prevent extent of ventricular aneurysm formation
which 3 drugs decrease demand beta blockers-NTG-morphine
which 6 thinigs increase supply 02-ASA (antiplatelet)-thrombolytics (clot busters)-Ntg (vasodilator)-morphine-PCI/CABG
what is a PCI stent or CABG
which artery is the widow maker artery the LAD
when teaching a pt about a MI what is an important thing to tell them when they have the pain to sit down-take 1 nitro and if the pain does not go away take another one (take the nitro q 5 mins) if the pain has not gone away after 3 then call 911
what are the 4 primary things that beta blockers do decrease HR-decrease BP-decrease contractility-protect the heart from over work
what 3 drugs increase HR atropine-epi-dopamine
what 4 drugs decrease HR beta blockers-ca chanel blockers-morphine and dig
what increases prelaooad IV volume therapy
what 3 things decrease preload nitrates-diuretics-morphine
what 5 things decrease afterload ca chanel blockers-ace inhibitors-nipride-dobutamine
what 5 drugs (not the classes) increase contractility digoxin-dopamine-dobutamine-PDE's-epi
what 2 drug classes decrease contractility beta blockers-morphine
why do we decrease contractility it protects the heart by decreasing workload and decreases 02 demand and consumption
what are the 3 things affected with cardiogenic shock primary ventricular ischemia-structural and arrhythmias
what is at the very bottom of the cascade of the cardiogenic shock diagram impaired cellular metabolism
what happens exactly with the metabolism our bodies like aerobic metabolism but when we have impaired cellular metabolism our bodies become anaerobic metabilism and there is a build up of lactic acid
can we treat cardiogenic shock no - there is little to no response to treatment
why do we not treat because of the loss of muscle mass you can't make the dead tissue come back
when someone is in cardiogenic shock what is the CO like less than 4L/min
what is the CI like less than 2.2/L/min
what is the PAWP like greater than 18
in the end what happens to organs in the body with cardiogenic shock they are not getting perfussed
what happens to urine output decreased
what happens to breathing tachypnea
what are lung sounds like adventitous
what are heart sounds like there are extra heart sounds
what is skin like (3) cyanosis, palor, cool clammy skin
what is the key cause of cardiogenic shock acute MI
how much of the muscle mass is usually lost 40% or more
with cardiogenic shock what is perfussion like to the coronaries very poor to the coronaries
what is CO and bp like with cardiogenic shock decreased
what is bp like with cardiogenic shock decreased
what is the number 1 goal with cardiogenic shock restore flow to the coronaries
what are 2 ways we can do this IABP or VAD
what do we want to see the LVEDP at for someone with cardiogenic shock 18
what drugs can we use on someone with cardiogenic shock to increase contractility (class) positive ianotropes
what do we want to do with afterload on someone with cardiogenic shock decrease igt
what do we want to do with arrhythmias on someone with cardiogenic shock control them
what does dobutamine help with and what does it do to SVR contractility and decreases SVR
what does dopamine do in regards to constriction vasoconstriction
what kind of effect does dopamine have a positive Ionotrope effect
what drug bronchodilates and vasoconstricts epinephrine
what type of drug is epinephrine positive ionotrope
which drug is a positive inotrope and also a vasodilator phosphodiesterase inhibitor
which side does ntg dilate the venous
which side does nipride dilate the arterial
**note: morphine is a potent venodilator
what are the 2 types of CABG SVG (stavenous venous graft) and LIMA (left internal mammary art)
what do you call a bypass that is minimally invasive MIDCABG
how long does a LIMA usually last 10-15 yrs
how long does a SVG last 5-10 yrs
what is one other thing other than the surgery that can improve patency ASA-80-325 mg
patency to some degree is also up to the patients lifestyle changes-do they change their diet and exercise after the surgery??
post op mngmnt of a CABG-how long is the pt usually in ICU 24-48 hrs
how often is an assessment done on the pt usually q 15 min to hourly
they usually have chest tubes, Iv's, foley, arterial lines
what types of things can we as nurses help the pt to do after CABG surgery TCDB-dangle-walk
the pt is usually sent home how long after surgery 4-6 days
what are 6 complications that can happen post op CABG decrease CO/CI-cardiac tamponade-arrhythmias-emboli-CVA-fluid volume excess
what is one thing we can do to help the pt with the increase in fluid volume excess up and walking
what is something that can cause the decreased CO and low CI post op CABG arrythmias or low volume
with a decreased CI post op CABG the HR may be too fast or too slow - how can we treat this (2 ways) pace or stimulate/slow with drugs
what is one way we could treat the decreased preload post op CABG give volume (the wedge would be high)
what is one way we could treat the increased preload post op CABG give lasix (the wedge would be low)
what is one way we could treat increased afterload post op CABG give Nipride to decrease the SVR
what are 4 drugs we can give to decrease contractility dopamine-dobutamine-Inocar and Epi (DIED)
a build up of blood or other fluid in the pericardial sac which puts pressure on the heart which then may prevent it from pumping effectively cardiac tamponade
what is the main complication of post op CABG arrythmias
what 3 things does TCDB and walking help with post op CABG oxygenate, preventing clots, move fluid back to the vascular tree
post op CABG a person may get third spacing fluid build up - what can you do for this person to help with this (3) keep the legs elevated-diuris and walk walk walk
what can you tell the person this is from fluid shift after surgery
you may see a wt gain of 7-10 lbs in this person because of the fluid shift
what will happen to the gas exchange because of the fluid altered
what is cardiomyopathy big old floppy heart
what is the EF of a floppy heart usually <35
what is the cause of a floppy heart unknown
what is the number one goal of someone with a floppy heart increase the cardiac output
there are 3 types of cardiomyopathy-which one is the one we are dealing with dilated
what are the 3 characteristics of dilated cardiomyopathy ventricular dilation, impaired systolic function and stasis of blood in LV
what is the bad thing about the blood stasis in the LV it could clot and then break off and cause a PE or stroke
what are 13 symptoms someone may show if they have a floppy heart decreased act tolerance-fatigue-dry cough-dyspnea-PND-palpitation-anorexia-s3/s4-hepatomegaly-JVD-systemic embolization
what is the reason for the fatigue they are not perfusing enough
what is the one thing that may be the 1st symptom of heart failure dry cough
what is the reason for the hepatomegally the blood is backing up and causing this
care of someone with cardiomyopathy -what do we want to do to the contractility enhance it (improve it)
what do we want to protect the ventricle
what do we want to do with afterload decrease it
what sometimes happens with synchronization in people with cardiomyopathy it is off
what do they have to do to this bi ventricular pacemaker to improve the synchronization
what are the 6 drugs used for someone with cardiomyopathy dig-ace inhibitors-beta blockers-diuretics-dobutamine or phosphodiesterase inhibitors-coumadin
what is the electrical pathway of the heart SA node-intercostal pathways-AV node-bundle of HIS-Purkinje fibers
what does the P wave on an EKG represent atrial contraction
what is the PR on the EKG the heart is resting
what is the QRS on the EKG ventricular contraction
initiate impulse without external stimulus automaticity
reach a threshold in response to stimulus excitability
propagate an impulse cell to cell conductivity
muscle cells shorten in response to stimulus contractility
which system slows down the SA and AV nodes and decrease contraction parasympathetic
which system speeds the SA and AV nodes up sympathetic
what are the 2 things that affect the mechanisms of arrhythmias 1-disorder of impulse formation at the SA node (gets like this if it is irritated) 2-length of refractory periods (rest)
which wave on the EKG is the rest period or refractory period **T wave is the rest period
a 12 lead EKG reflects electrical activity from where all different positions
how long should the PR interval be on a normal rhythm 0.12 - 0.20
how long should QRS be 0.04 - .12
how long should the QT inerval be 0.34 - 0.43
how do you calculate the HR by looking at a strip HR X the number of R-R intervals
which cells in the heart act as a pacemaker ALL the cells in the heart can act as pacemaker cells
what is the primary pacer of the heart the SA node
what is the rate of the SA node set to usually for a normal heart 60-100
what is the rate at which other parts of the atria pace the heart at 60-100
what is the rate at which the AV node paces the heart 35-60
at what rate does the ventricle pace the heart less than 40
if you only had impulses from the ventriccle and NOT the atrium what would you be missing on a EKG reading the P wave (because the P wave is the atrium contracting)
what kind of beats occur if the SA node is pacing too slowly escape beats
what do you call beats that occur where they are not suppossed to occur ectopic beats-usually secondary pacer sites discharge faster than the SA node
when evaluating arrhythmias we have to do it in a systematic approach - what is the order in which we evaluate rate-rhythm-P wave present-P wave for each QRS?-QRS for every P-QRS width-PR interval
with a heart beat you have electrical first followed by mechanical
what is artifact some kind of outside interferrence
with sinus brady what is the heart rate like less than 60-everything else is normal
what is 1 thing that sinus brady can be caused by Hypoxia
what does treatment usually depend on patient tolerance
what are 2 things that we can use to treat sinus brady atropine or pacing
with sinus tachy what is the HR like greater tha n 100 - everything else normal
with sinus tachy what happens to the 02 there is an increase in consumption
what are 3 drugs they can give to help with sinus tachy beta blockers, ca chanel blockers and digoxin
which rhythm is grossly irregular with no identifyable P wave A-fib
what is one other thing that is lost with A fib the atrial kick - because there is no P wave (atrial contraction)
with A-fib there is also a loss in CO of how much 25-30%
because of this loss of CO what may happen to the blood in the atria it may clot
what is there an increase with increase chance of CVA - 5 fold
what medicine do they use a lot in someone with A-Fib coumadin
what is the treatment goal for someone with a-fib to decrease ventricular responses (because you have ventricular chaos)
what 4 drugs can do this dig-beta blockers-ca channel blockers and antiarrhythmics
what is the other thing other than drugs that they can do for A-fib cardioversion
what rhythm looks like sawtooth waves atrial flutter
with atrial flutter are there any P waves no
is there a QRS yes - normal
what is the rate usually like for someone with atriall flutter usuallly around 150 bpm
can atrial flutter decrease CO yes
what is the goal with atrial flutter to slow ventricular response
what do you need to do in an emergency situation for someone with atrial flutter ccardiovert them
what drugs would you use to help someone in atrial flutter same as A-fib-dig-beta blockers-ca channel blockers and antiarrhythmics
wide distorted bizzarre QRS with no P wave PVC
is there decrease CO with PVC's yes
when do we become concerned with PVC's if there are more than 6 per minute
what 6 things are PVC's associated with hypokalemia-hypokia-ischemia-caffine-alcohol-drugs
when is an instance other than those above that PVC's may occur after clot lysis (reperfusion arrhythmias)
what is it called if you have 2 PVC's in a row couplet
what is it called if you have 3 PVC's in a row triplet
if you have more than 3 PVC's in a row what do we call this ventricular tachycardia
if you have a PVC every other beat what is this called Bigeminy
what is the HR if someone is in V-tach 110-250
are there any P waves with V-tach no
with v tach do you have any CO only a little bit
why is this there is a low filling time and loss of atrial contraction (esp if sustained more than 30 seconds)
what can V-tach quickly deteriorate to V-fib
what are the 2 drugs they use for v-tach amiodorone or lidocaine if the pt is stable
if the pt has no pulse in v-tach what do you need to do defribillate
if you see a fibrillatory wave only as ventricles are quivering on the EKG what is this V-fib
do you have a CO with V-fib NO
what is the pt usually like when theey are in V-fib unconsciouss-no pulse-no respirations
what should you do if a pt is found like this CPR until defribillator-stop to defibrillate-cpr for 2 mins
what should also be given during CPR IV epinephrine
if there is absence of any ventricular activity what is this asystole-flat line
*****with asystole you may see just P waves but that is alll******
non-traumatic cardiac arrest with return of spontaneous circulation (ROSC) induced hypothermia
what is the time to initiation less than 6 hrs
is the pt awake after ROSC no usually comotosed
what is their Glascow coma scale like usually less than 8
what is something that EMS can give to initiate the induced hypothermia chilled IV NS
**the heart is chilled x24 hrs then slowly rewarmed over the next 48 hours
what do we need to know about 3rd degree heart block it is bad and does not go away on its own
**NOTE-just know that there are 6 different classes of antiarrhythmics and they all work differently
Created by: tiglets