213 Exam 1 - O'Neal
Quiz yourself by thinking what should be in
each of the black spaces below before clicking
on it to display the answer.
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| after you exercise what happens to your o2 demand | it increases
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| does an increase in your demand increase your o2 supply | yes
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| in what way does your body compensate for an increase in o2 supply and demand | it increases your HR
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| what is it called - how much blood volume is going out per stroke | stroke volume
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| does your stroke volume change during little exercise | no - just your HR increases
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| with a hr of up to about 132 bpm your heart has enough time to fill with the same volume (amnt of blood) |
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| what is the formula for cardiac output | HR x Stroke volume
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| 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
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| 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.
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| 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
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| which ventricle would use up more 02-one with 150 pressure or one with 120 | 120
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| what is a normal diastolic pressure in the ventricle | 6-12
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| what happens during diastole in the ventricle | the coronary artery will fill
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| diastole is when the ventricle relaxes so that it can fill |
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| what is cardiac output approx | 4-8 L/min
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| 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.
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| what is cardiac index | the amnt of perfusion per body service area
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| what is a normal cardiac index | 2.2 or higher
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| June probably had a higher cardiac index |
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| % of total volume being ejected into the body | ejection fraction
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| what is a normal ejection fraction | 50-70%
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| 4 determinants of cardiac output are | HR-preload-afterload-contractility
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| 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)
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| on a chest x-ray if you see black what is this | air
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| what do you see on a chest xray if there is fluid | white
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| if the pulmonary vasculature is congested what does this mean | there is too much fluid (blood)
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| if you get to a point where you have too much fluid and it leaks out then what do you get | pulmonary edema
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| 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
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| when are other situtions when BNP is high | angina-hypotensive-MI-LV hypertrophy
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| if HR is up is CO up | yes
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| if HR is up is CO down | it could be if the person was severly tacchy
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| if HR is down is CO down | yes
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| 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.
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| 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
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| you need to know WHAT CAUSED IT-it maybe meds or the pt may be an athlete |
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| preload-what does preload reflect | volume which reflects workload
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| the heart is the most full at the end of what | diastole
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| 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
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| when does the heart have the highest pressure | when it's the most full - (at the end of diastole)
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| 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
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| 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.
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| what 2 pressures has research shown to be the same | PA and LVEDP
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| 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
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| 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
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| where is the tip of a central located | superior vena cava right outside the rt atrium
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| what pressure can that get us | CVP (it's closer to the rt side - venous side of the heart)
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| which side of the heart does a catheter tell us most about | the side that it is closest to or the opposite side
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| which 2 pressures are more specific to the left side of the heart | cap wedge or LVEDP
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| Initially which side of the heart fails | the L side
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| usually the right side of the heart will fail because the l side has failed |
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| what do diuretics get rid of | pulmonary congestion
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| what happens to pressure as volume increases | it increases
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| what happens to pressure as volume decreases | it decreases
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| what is a normal LVEDP | 6-12
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| what is a normal PAWP | 6-12
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| what is a normal PA diastolic pressure | 6-12
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| what is a normal CVP | 4-6
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| 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
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| why is a wedge not good for a pt | because it can cut off o2 supply
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| what does too much pressure do to the heart | it makes the heart back up
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| 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
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| 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
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| what is the primary function of a pulmonary artery catheter | to help evaluate L ventricular pressure/volume and function
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| if I have a big old floppy heart does it need more volume than a normal hear | yes
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| what is a floppy heart called | a sick heart
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| what is the EF usually for a sick heart | <35
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| 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
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| what would someone probably be on as a standing order if they had a sick heart | lasix-because they have more volume
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| what does Starlings law say | the more the heart is filled during diastole the more forcefully it contracts like stretching a rubber band
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| 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
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| increased volume results in what 3 things | increased stretch, stroke volume, cardiac output
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| If our preload decreases then what happens to out volume | it decreases
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| 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
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| what are 4 things that decrease preload (volume) | bleeding, diuresis, venous dilation(decreases flow coming into the heart) - arterial dilation
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| if you were giving a drug would you try to dilate the venous or arterial side | venous-because
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| what are 3 drugs we give to diuresis | lasix, diuril and bumex
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| what drugs vasodilate the venous system | nitroglycerin
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| is there an actual change in the amnt of volume when preload is decreased by vasodilation | no - it is just re-distributed
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| BUN |
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| Creatinine |
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| sodium |
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| potassium |
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| glucose |
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| chloride |
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| Co2 |
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| what is afterload | its basically the force that is needed for the heart to eject the blood to the body
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| is afterload venous or arterial | arterial
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| how is afterload measured | SVR-systemic vascular resistance
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| what is a normal SVR number | 800-1200
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| 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 |
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| increased afterload = increase in forces opposing ventricular ejection |
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| what does an increased afterload do to CO | decreases it
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| T or F - increased afterload decreases cardiac output | t
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| T or F - increased afterload makes the heart work harder | T
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| T or F - increased afterload increases oxygen demand | T-because the heart is working harder
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| T or F - increased afterload increases oxygen consumption | T
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| 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
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| what happens if you are overworking your heart and it can't pump forward properly | it backs up
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| to increase cardiac output what can we do to afterload | decrease it
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| decreased afterload does what to 02 demand and consumption | it decreases it
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| what does a decreased afterload do to cardiac output | it increases it
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| what are 2 ways that we can decrease afterload | decrease SVR or give arterial vasodilators
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| what are 4 arterial vasodilators | ACE inhibitors, ARB's, Ca channel blockers and Nipride (Nipride is a very potent vasodilator given IV)
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| what is a venous dilator | nitrates
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| increased contractility means what for CO | increased
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| what are some ways we can increase contractility of the heart | positive Ionotropes, beta adrenergic agonists, phosphodiesterase inhibitors
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| what do positive Ionotropes exactly do to the heart | help it squeeze better
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| what is a positive Ionotropes | Digoxin,
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| what are some s/s of digoxin toxicity | anorexia, n/v, visual disturbances, (halo, yellow vision) arrithmias
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| what are 3 beta adrenergic agonists | dopamine, dobutamine, epi
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| what 2 things do phosphodiesterase inhibitors do | increase contractility and decrease afterload
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| why should we decrease contractility (2) | it protects the heart by decreasing work load and decreases 02 consumption and demand
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| what drugs decrease contractility | beta blockers
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| what are the 2 most common circulatory assist devices | IABP (Intra aortic balloon pump and VAD-(ventricular assist device)
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| what 2 things does a IABP do | decreases afterload and increases coronary perfusion (remember Youtube video)
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| when is a VAD used | until the heart recovers or a donor is found
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| what are 3 drugs that decrease HR | beta blockers, Ca chanel blockers, digoxin
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| what are 2 drugs that decrease preload | diuretics and venous dilators such as ntg
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| what are 4 drugs that decrease afterload | ACE inhibitors, ARBS, Arterial dilators like Nipride and Ca Chanel blockers
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| what are 2 types of drugs that increase contractility | positive ionotropes and phosphodiesterase inhibitors
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| what are 4 positive ionotropes | digoxin, dopamine, dobutamine, epinephrine
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| what are 2 phosphodiesterase inhibitors | Inacor and Primacor
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| what 3 things to beta blockers do | decrease HR, decrease BP and decrease contractility
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| what 4 things do Ca Chanel blockers do | vasodilate (arterial)-Decrease BP-decrease HR-decrease afterload
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| what 3 things do ACE inhibitors do | vasodilate (arterial)-decrease BP-decrease afterload
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| what 4 things do ARBs do | block the action of angiotensin II- vasodilate (arterial)-decrease BP-decrease afterload
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| review coronary arteries - L, R, Left anterior descending and L circumflex |
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| comes from an incomplete obstruction | angina
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| comes from a complete obstruction | infarction
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| across the wall of the heart muscle-it gets all layers of the heart | transmural MI
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| just involves 1 layer of the heart | subendocardial MI
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| which one is worst - transmural or subendocardial | transmural
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| a MI will more than likely occur if there is ischemia to the heart for how long | more than 20 minutes
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| it involves cell death and tissue necrosis |
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| review name and location of MI's - anterior, inferior, lateral, septal |
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| healing process of an MI - what are release in the first 24 hrs after an MI | enzymes
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| what happens after 6 hrs | physical changes
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| necrotic tissue removal happens how long after an MI | 2-3 days
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| when is necrotic tissue replaced by scar | 6 weeks after the MI
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| when is a thin walled firm scar formed | 2-3 months
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| what is it called if it is dead, scarred, and cannot be helped | infarction
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| what is it called if it is swollen, but can heal and must be protected | injured
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| what is it when there is no permanent damage unless prolonged | ischemic
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| angina pain or MI pain- substernal or elsewhere | angina or MI
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| precipitated by stress or exertion | angina
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| relieved by NTG or rest | angina
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| lasts >30 mins | MI
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| may occur without cause | MI
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| pattern: stress, pain, rest, relief | angina
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| usually not relieved | MI
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| usually have associated symptoms | MI
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| what are some of the associated symptoms | n/v, epigastric pain, arrhythmias, s3 or s4, fever, crackles, jvd, decreased UO, fear, SOB, sweating
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| what are the 3 things that have to be present for an MI | clinical presentations, serum cardiac markers, EKG changes
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| what are some of the cardiac markers seen after someone has a heart attack | CK or CPK - CK MB bands - Toponin
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| which one is specific to cardiac muscle | CK MB bands
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| which one is the MOST specific to cardiac muscle | Troponin
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| when do ck levels rise | in 3-12 hrs
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| when do CK levels peak | in 24 hrs
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| when do CK levels go back to normal | in 2-3 days
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| how do they draw the CK MB bands | in a series of 3 - and drawn 6 hrs apart
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| **** NOTE to confirm a HA ALL 3 cardiac enzymes need to be elevated. |
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| if CK is normal and MB is elevated has the pt had a HA | no
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| when do we suspect a HA | if MB and troponin are both elevated.
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| if there is an ST elevation what does this mean | infarction
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| if there is an ST depression what does this mean | ischemia
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| what does Q wave mean | old infarction
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| what does MONA stand for | morphine, oxygen, nitro, asprin
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| what are some other dx measures for an MI | elevated WBC count, Thallium scan, blood glucose,
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| 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)
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| FACT-80-90% of MI's are secondary to a thrombus |
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| what is the main goal | to salvage as much muscle as possible
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| when is the only time we like to see arrhythmias | when there has been immediate reprefussion
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| 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
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| 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)
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| 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
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| what is the most common complication of a heart attack | arrhythmias
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| what is the "King" of antiarrhythmia drugs | Amiodorone
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| what is one other drug they use to treat arrhythmias | lidocaine
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| do they usually treat arrhythmias | no - only if they are sustained and life threatning
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| 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
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| what can morphine do to respirations | depress them
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| what kind of drug is ASA | an antiplatelet
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| what 3 things do beta blockers do when you are giving them with an MI | decrease HR-decrease contractility-some decrease preload
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| what 2 things do ACE inhibitors/ARBS do | decrease afterlaod-help prevent extent of ventricular aneurysm formation
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| which 3 drugs decrease demand | beta blockers-NTG-morphine
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| which 6 thinigs increase supply | 02-ASA (antiplatelet)-thrombolytics (clot busters)-Ntg (vasodilator)-morphine-PCI/CABG
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| what is a PCI | stent or CABG
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| which artery is the widow maker artery | the LAD
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| 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
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| what are the 4 primary things that beta blockers do | decrease HR-decrease BP-decrease contractility-protect the heart from over work
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| what 3 drugs increase HR | atropine-epi-dopamine
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| what 4 drugs decrease HR | beta blockers-ca chanel blockers-morphine and dig
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| what increases prelaooad | IV volume therapy
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| what 3 things decrease preload | nitrates-diuretics-morphine
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| what 5 things decrease afterload | ca chanel blockers-ace inhibitors-nipride-dobutamine
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| what 5 drugs (not the classes) increase contractility | digoxin-dopamine-dobutamine-PDE's-epi
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| what 2 drug classes decrease contractility | beta blockers-morphine
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| why do we decrease contractility | it protects the heart by decreasing workload and decreases 02 demand and consumption
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| what are the 3 things affected with cardiogenic shock | primary ventricular ischemia-structural and arrhythmias
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| what is at the very bottom of the cascade of the cardiogenic shock diagram | impaired cellular metabolism
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| 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
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| can we treat cardiogenic shock | no - there is little to no response to treatment
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| why do we not treat | because of the loss of muscle mass you can't make the dead tissue come back
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| when someone is in cardiogenic shock what is the CO like | less than 4L/min
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| what is the CI like | less than 2.2/L/min
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| what is the PAWP like | greater than 18
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| in the end what happens to organs in the body with cardiogenic shock | they are not getting perfussed
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| what happens to urine output | decreased
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| what happens to breathing | tachypnea
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| what are lung sounds like | adventitous
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| what are heart sounds like | there are extra heart sounds
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| what is skin like (3) | cyanosis, palor, cool clammy skin
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| what is the key cause of cardiogenic shock | acute MI
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| how much of the muscle mass is usually lost | 40% or more
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| with cardiogenic shock what is perfussion like to the coronaries | very poor to the coronaries
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| what is CO and bp like with cardiogenic shock | decreased
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| what is bp like with cardiogenic shock | decreased
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| what is the number 1 goal with cardiogenic shock | restore flow to the coronaries
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| what are 2 ways we can do this | IABP or VAD
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| what do we want to see the LVEDP at for someone with cardiogenic shock | 18
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| what drugs can we use on someone with cardiogenic shock to increase contractility (class) | positive ianotropes
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| what do we want to do with afterload on someone with cardiogenic shock | decrease igt
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| what do we want to do with arrhythmias on someone with cardiogenic shock | control them
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| what does dobutamine help with and what does it do to SVR | contractility and decreases SVR
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| what does dopamine do in regards to constriction | vasoconstriction
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| what kind of effect does dopamine have | a positive Ionotrope effect
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| what drug bronchodilates and vasoconstricts | epinephrine
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| what type of drug is epinephrine | positive ionotrope
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| which drug is a positive inotrope and also a vasodilator | phosphodiesterase inhibitor
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| which side does ntg dilate | the venous
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| which side does nipride dilate | the arterial
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| **note: morphine is a potent venodilator |
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| what are the 2 types of CABG | SVG (stavenous venous graft) and LIMA (left internal mammary art)
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| what do you call a bypass that is minimally invasive | MIDCABG
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| how long does a LIMA usually last | 10-15 yrs
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| how long does a SVG last | 5-10 yrs
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| what is one other thing other than the surgery that can improve patency | ASA-80-325 mg
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| patency to some degree is also up to the patients lifestyle changes-do they change their diet and exercise after the surgery?? |
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| post op mngmnt of a CABG-how long is the pt usually in ICU | 24-48 hrs
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| how often is an assessment done on the pt | usually q 15 min to hourly
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| they usually have chest tubes, Iv's, foley, arterial lines |
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| what types of things can we as nurses help the pt to do after CABG surgery | TCDB-dangle-walk
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| the pt is usually sent home how long after surgery | 4-6 days
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| what are 6 complications that can happen post op CABG | decrease CO/CI-cardiac tamponade-arrhythmias-emboli-CVA-fluid volume excess
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| what is one thing we can do to help the pt with the increase in fluid volume excess | up and walking
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| what is something that can cause the decreased CO and low CI post op CABG | arrythmias or low volume
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| 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
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|
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| what is one way we could treat the decreased preload post op CABG | give volume (the wedge would be high)
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| what is one way we could treat the increased preload post op CABG | give lasix (the wedge would be low)
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|
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| what is one way we could treat increased afterload post op CABG | give Nipride to decrease the SVR
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|
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| what are 4 drugs we can give to decrease contractility | dopamine-dobutamine-Inocar and Epi (DIED)
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| 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
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|
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| what is the main complication of post op CABG | arrythmias
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|
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| what 3 things does TCDB and walking help with post op CABG | oxygenate, preventing clots, move fluid back to the vascular tree
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|
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| 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
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| what can you tell the person this is from | fluid shift after surgery
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| you may see a wt gain of 7-10 lbs in this person because of the fluid shift |
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| what will happen to the gas exchange because of the fluid | altered
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|
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| what is cardiomyopathy | big old floppy heart
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|
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| what is the EF of a floppy heart | usually <35
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|
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| what is the cause of a floppy heart | unknown
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|
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| what is the number one goal of someone with a floppy heart | increase the cardiac output
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|
||||
| there are 3 types of cardiomyopathy-which one is the one we are dealing with | dilated
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|
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| what are the 3 characteristics of dilated cardiomyopathy | ventricular dilation, impaired systolic function and stasis of blood in LV
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|
||||
| 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
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|
||||
| 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
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|
||||
| what is the reason for the fatigue | they are not perfusing enough
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|
||||
| what is the one thing that may be the 1st symptom of heart failure | dry cough
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|
||||
| what is the reason for the hepatomegally | the blood is backing up and causing this
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|
||||
| care of someone with cardiomyopathy -what do we want to do to the contractility | enhance it (improve it)
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|
||||
| what do we want to protect | the ventricle
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|
||||
| what do we want to do with afterload | decrease it
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|
||||
| what sometimes happens with synchronization in people with cardiomyopathy | it is off
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|
||||
| what do they have to do to this | bi ventricular pacemaker to improve the synchronization
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|
||||
| what are the 6 drugs used for someone with cardiomyopathy | dig-ace inhibitors-beta blockers-diuretics-dobutamine or phosphodiesterase inhibitors-coumadin
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|
||||
| what is the electrical pathway of the heart | SA node-intercostal pathways-AV node-bundle of HIS-Purkinje fibers
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|
||||
| what does the P wave on an EKG represent | atrial contraction
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|
||||
| what is the PR on the EKG | the heart is resting
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|
||||
| what is the QRS on the EKG | ventricular contraction
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|
||||
| initiate impulse without external stimulus | automaticity
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|
||||
| reach a threshold in response to stimulus | excitability
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|
||||
| propagate an impulse cell to cell | conductivity
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|
||||
| muscle cells shorten in response to stimulus | contractility
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|
||||
| which system slows down the SA and AV nodes and decrease contraction | parasympathetic
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|
||||
| which system speeds the SA and AV nodes up | sympathetic
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|
||||
| 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)
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|
||||
| which wave on the EKG is the rest period or refractory period | **T wave is the rest period
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|
||||
| a 12 lead EKG reflects electrical activity from where | all different positions
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|
||||
| how long should the PR interval be on a normal rhythm | 0.12 - 0.20
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|
||||
| how long should QRS be | 0.04 - .12
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|
||||
| 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
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|
||||
| 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
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|
||||
| what is the rate of the SA node set to usually for a normal heart | 60-100
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|
||||
| what is the rate at which other parts of the atria pace the heart at | 60-100
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|
||||
| what is the rate at which the AV node paces the heart | 35-60
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|
||||
| 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)
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|
||||
| what kind of beats occur if the SA node is pacing too slowly | escape beats
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|
||||
| 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
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|
||||
| 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
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|
||||
| with a heart beat you have electrical first followed by mechanical |
🗑
|
||||
| www.youtube.com/watch?v=Q0MfIVaDUE&nofeather=True |
🗑
|
||||
| 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
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|
||||
| 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
🗑
|
||||
| *******NOTE - TREATMENT IS DETERMINED BY THE UNDERLYING CAUSE************ |
🗑
|
||||
| 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)
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|
||||
| with A-fib there is also a loss in CO of how much | 25-30%
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|
||||
| 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 |
🗑
|
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