213 Exam 1 – O’Neal

Question Answer 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 sat_flash_1 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 BUN Creatinine sodium potassium glucose chloride Co2 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 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 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) 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

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