BC3 cardiac lecture 1/22/08
Help!
|
|
||||
|---|---|---|---|---|---|
| coagulation studies | PTT and the INR
🗑
|
||||
| on anticoagulant if ? | had an MI
🗑
|
||||
| Heparin works on what cascade | intrinsic cascade
🗑
|
||||
| Coumadin works on what clotting cascade | extrinsic cascade
🗑
|
||||
| Intrinsic clotting cascade starts at what factor? | V through XII
🗑
|
||||
| extrinsic clotting cascade starts at factor | VII
🗑
|
||||
| common pathway of clotting cascade at ? | factor X
🗑
|
||||
| Therapeutic PTT is ? | 2 to 2 1/2 times normal
🗑
|
||||
| normal PTT is | 25
🗑
|
||||
| therapeutic where you want your patience to be is ? | between 45 and 70,that’s 45 to 70 seconds for that blood clot
🗑
|
||||
| Why in the world would we want that blood to take 45 to 70 seconds to clot when 25 is normal? | Because they are on an anticoagulant-something to prevent clotting.
🗑
|
||||
| An INR is normally around | 1.1, 1.2
🗑
|
||||
| Therapeutic INR on Coumadin would be about ?? depending on why the patient is on it. | 2-3,
🗑
|
||||
| if they have a heart valve , keep INR between | 2.5 and I believe 3.5; on coumadin
🗑
|
||||
| if you have metal, put in a patient - metal causes | clots
🗑
|
||||
| therapeutic anticoagulation level | running your INR high due to circumstnaces, IE, they have metal in
🗑
|
||||
| hypokalemia. norm K+ 3.5 to 5.3 | causes can be vomiting, Diarrhea,Prolonged diuretic therapy – lasix ,some cardiac dysrhythmias if they don’t have enough potassium, a U wave,PVC’s, V-tach, V-fib or death.
🗑
|
||||
| hyperkalemia, norm K+ 3.5 to 5.3 | from Addison's disease, acute renal failure, Acidosis ,
🗑
|
||||
| potassium level of greater than 6-7. | Tall tented T wave on ECG, almost as high as QRS
🗑
|
||||
| treat hyperkalemia | use of potassium sparing diuretics,dialysis
🗑
|
||||
| Hyperkalemia, you can have What on ECG's | elevated T wave, sinus brady,first degree AV block, V-fib, V-tach or sudden death
🗑
|
||||
| Does potassium play a role in a CABG | stops the heart; cardiac standstill
🗑
|
||||
| Calcium norm is usually? | 8-11; 9-11
🗑
|
||||
| hypercalcemia on ECG | shortening of the QT wave
🗑
|
||||
| calculate the QT interval | Punch in the QT interval hit the divided sign punch in the RR interval, hit the square root sign and hit equal
🗑
|
||||
| What would cause hypercalcemia? | Hyperparathyroidism, and any kind of neoplastic disease : cancer
🗑
|
||||
| Causes Hypocalcemia | renal failure, hypoparathyroidism or a malabsorption syndrome.
🗑
|
||||
| EKG with hypocalcemia | prolonged or lengthened QT interval
🗑
|
||||
| Lipid studies; good cholesterol | HDL, it is about 30% of your total cholesterol and it is considered to be protective want greater than 35
🗑
|
||||
| Total cholesterol level should be | below 200
🗑
|
||||
| LDL should be | less than 130 / if heart diseasse,less than 100
🗑
|
||||
| Triglycerides | want those to be less than 200
🗑
|
||||
| if Triglycerides are high? pt. has | increased, the patient tends to have more atherosclerosis and CAD, coronary artery disease.
🗑
|
||||
| enzymes | creatinine kinase or creatinine kinase MB, LDH and troponin;normally contained in an intact cell
🗑
|
||||
| enzymes are found in blood when | cell wall becomes damaged, the cell wall opens up and releases the enzymes;That’s why you can find them in the blood work.
🗑
|
||||
| damaged cells yield | enzymes; creatinine kinase or creatinine kinase MB, LDH and troponin
🗑
|
||||
| enzymes that can be found in blood work determine? | if the patient has had an MI.
🗑
|
||||
| CKMB specific to | the heart
🗑
|
||||
| CK MB is an? | isoenzyme, or a portion of the total CK
🗑
|
||||
| CK is broken down into | CKMB, CKBB and CKMM. MM is muscle , BB Brain, MB heart
🗑
|
||||
| Your CKMB is elevated | depending on the amount of cellular damage. If one cell is disrupted, you have a little bit; if you have a very large infarct,CKMB is elevated even more; dependent on the amount of necrosis and cellular damage
🗑
|
||||
| enzymes peak and decline at different time periods and that is important because ? | helps us pinpoint when the MI has occured.
🗑
|
||||
| Your CK goes up and it comes down very quickly, up and down in -______ ? days | elevates and comes down in 3 days
🗑
|
||||
| we use other enzymes that stay elevated for a longer period of time to help us determine if the patient is having a MI. | Troponin
🗑
|
||||
| a Q wave MI | Q wave never goes away – 1/3 of the total R wave
🗑
|
||||
| inverted T wave? | little bit of ischemia
🗑
|
||||
| isoenzymes | CKMM; CKMB; CKBB ; AST: LDH they go up and down depending on damage.
🗑
|
||||
| Troponin – elevated for | 14 days
🗑
|
||||
| LDH is an enzyme | distributed through the body through the liver; kidney, the heart and it is in the lungs
🗑
|
||||
| when we look at LDH we look at ? | looking at LD1 and LD 2 for heart disease
🗑
|
||||
| LDH ratio. | The ratio of LD1 to LD2 is less than 1
🗑
|
||||
| a flipped ratio | LD2 is greater than the LD1.accurate in 80% of your MI’s. do LDH with a CPK.
🗑
|
||||
| LDH.how long is it elevated ? | up to 12 days
🗑
|
||||
| AST and your ALT | liver enzymes: if the AST is 3 times greater than your ALT that tells you that the etiology is cardiac. problem is cardiac
🗑
|
||||
| Troponin. | Troponin is one of the 3 proteins that make up the troponin complex. Troponin T and Troponin I.
🗑
|
||||
| Cardiac Troponin T has been shown to be elevated in all patient’s within how long of HA? | 4 hours of cardiac damage and stays elevated for up to 14 days
🗑
|
||||
| Troponin also elevated in ? | unstable angia
🗑
|
||||
| does NOT go up with unstable angina? | Creatinine, your AST, your ALT, your LDH,
🗑
|
||||
| serial enzymes | do them every 8 hours x 3 along with EKG every 8 hours x 3 to watch the evolution of the damage.
🗑
|
||||
| cardiac enzymes are used to:? | Predict the damage to the heart – the higher the level, the more cells involved, the more necrosis, the more heart damage.
🗑
|
||||
| BNP | use to determine if the patient has congestive heart failure;greater than 120,patient has CHF
🗑
|
||||
| when the left ventricle stretches, it releases? | BNP is captured in the blood, we do blood work, we see that it is elevated = CHF,careful: BNP also elevated in renal disease
🗑
|
||||
| CRP – C-reative Protein | predictive test that identifies inflammation and it is thought that many of the MI’s are due to the inflammatory process: high C-reative protein, that is predictive for an MI.
🗑
|
||||
| D-dimer | shows the end product of thrombus formation: has had a clot, his D-dimer would be elevated
🗑
|
||||
| Myoglobin | goes up quickly; within an hour, but it only stays elevated for 2-4 hours;not specific to the heart; released with any muscle damage.
🗑
|
||||
| Coronary angiography | assess the coronary arteries, they shoot dye, they can see the areas of occlusion if there are areas of occlusion. They will insert a stent or just dilate that area.
🗑
|
||||
| advance the catheter from the in cath lab | femoral vein to the vena cava and you can evaluate the right atrium, the tricuspid valve, the right ventricle and the pulmonary artery pressure.
🗑
|
||||
| a left heart cath | you advance the catheter through the femoral artery, you can check the AV – aortic valve, the mitral valve and you are looking for regurge or you are looking for stenosis.
🗑
|
||||
| electrophysiology studies | symptoms such as syncope, fluttering in the chest, irregular heart beat and what we do is we try to stimulate that irregular heart beat
🗑
|
||||
| Chest X-ray | evaluate the heart size ; heart is usually less than ½ the size of the diameter of the chest.
🗑
|
||||
| Holter monitor ; called an ambulatory EKG as well | portable EKG reporting device ;monitor your heart anywhere up to 48 hours. Along with that, you have to keep a diary. at 8:10 patient complained of heart fluttering feeling, lets look at the EKG at 8:10 – so they can compare the symptoms with the EKG
🗑
|
||||
| Electrocardiography, is used to | identify ejection fraction – wall motion
🗑
|
||||
| ejection fraction is? | percentage of blood that is ejected from the heart with each beat.
🗑
|
||||
| necrotic tissue is ? | scar tissue, less stretch, less movement
🗑
|
||||
| echocardiogram to identify | wall motion; also used to identify regurgitation.
🗑
|
||||
| echocardiogram to identify | Regurgitation from the left ventricle or right ventricle into the atria or from the vessels.
🗑
|
||||
| vegetation on the valves | bacterial endocarditis
🗑
|
||||
| mitral valve prolapse | prophylactic antibiotic: bacterial can go into the blood stream from dental work ; set up residency on the valves and that is called vegetation or subacute bacterial endocarditis.
🗑
|
||||
| can look for pericardial fluid and we can calculate the gradient | gradient gives us an indication of how much stenosis the valve actually has
🗑
|
||||
| echocardiogram M-Mode | very narrow view of the heart ; ice pick view
🗑
|
||||
| 2-D echo – that is more of a pie shape | more view of the heart; more visualization of the wall motion and the vegetation.
🗑
|
||||
| 2D echo, we also use it with exercise. | patient can exercise and we look for any heart abnormality during exercise;
🗑
|
||||
| persantine, dobutamine or cardiolyte | acts as a stressor to the heart, the same as when you exercise.
🗑
|
||||
| Doppler echo | assess the blood flow; looking for regurgitation at the valves.
🗑
|
||||
| Doppler echo | color-coded so that one way is blue, one way is red and they can tell the amount of regurgitation by the color of the blood. inject the bubbleslooking for is a break in the septal wall.So, you can have an atrial septal defect or a ventricular septal def.
🗑
|
||||
| TEE is a | transesophageal echocardiogram
🗑
|
||||
| transesophageal echocardiogram | sink a tube ;through the esophagus ;sits right next to the heart; good visualization of the left atrium
🗑
|
||||
| where many of your clots will form if your patient is in atrial fib. | left atrium because it has a left atrial appendage
🗑
|
||||
| Atrial fib | heart is not contracting well – it is not causing forward motion of the blood;stasis decreased because you loose your atrial kick
🗑
|
||||
| atrial kick | delivers up to 20% of your volume prior to closure of the valve. loose your atrial kick, as a result you do decrease your stroke volume.
🗑
|
||||
| Most of your clots will occur in | left atrium, behind that left atrial appendage; TEE, you can look for the clot
🗑
|
||||
| patient has a clot, would you want to reverse that dysrhythmia and put them in a normal sinus rhythym | NO; Send that clot to the BRAIN
🗑
|
||||
| clot in the brain is called | stroke
🗑
|
||||
| do a TEE and they see a clot | send the patient home on Coumadin for 4-6 weeks, keep him in atrial fib, bring him back in after 4-6 weeks, do another TEE ; clot is gone, then they can cardiovert him
🗑
|
||||
| prior to a TEE | NPO 6 hours ;mild sedative, probably Versed and they are NPO after the test until the gag reflex returns.
🗑
|
||||
| radionuclide imagining | Perfusion scans, perfusion imaging;shows how equal the uptake of the radioactive material tracer is; abnormal will have hot and cold spots
🗑
|
||||
| Cold spots | decreased tracer uptake and you can see that on a scanner;inject them; scan them;cold spot =decreased myocardial perfusion.
🗑
|
||||
| Hot spots | increased uptake= myocardial necrosis
🗑
|
||||
| ischemia – cold spot or hot spot? | cold spot, because it is decreased perfusion, decreased blood flow.
🗑
|
||||
| MI? Hot spot or cold spot? | Hot spot because an MI can go to necrosis if it is not treated
🗑
|
||||
| Severe ST elevation | having an MI
🗑
|
||||
| Nitro works 3 ways | decreases your preload, it decreases your afterload and it increases coronary artery perfusion
🗑
|
||||
| preload | venous return to the right side of the heart.
🗑
|
||||
| afterload? | pressure the left ventricle has to exert against the aorta to push out the stroke volume, or the ejection fraction.
🗑
|
||||
| Nitro is a | massive vaso-active agent that dilates both the superior and inferior vena cava and the aorta and the coronary arteries. It is short acting, but it is very quick acting.
🗑
|
||||
| what’s and alpha agent ( epinephrine) do? | vasoconstrict.blood pressure - it goes up
🗑
|
||||
| vaso-vagal response | stimulate vegus nerve/ parasympathetic/ lowers BP, and people can pass out
🗑
|
||||
| reversible perfusion uptake | you have decreased tracer uptake with exercise but returns to normal at rest
🗑
|
||||
| Fixed perfusion defect | decreased uptake at rest and exercise and there is no return to normal. This indicates a previous MI. With a fixed defect, patient has had a MI.
🗑
|
||||
| Thalium scans | another exercise stress test; every 3 minutes you increase the incline of the treadmill and you increase the speed of the treadmill until they reach a target heart rate.inject the thalium at peak exercise ;image again within 5 minutes of the inj.
🗑
|
||||
| Thalium scans/ hibernating MI. | Non-perfused areas have no thalium, they will be cold spots – this is called a hibernating MI.
🗑
|
||||
| Sestamibi Protocol | rest scan first;delay the imaging for 60 minutes ;that long for the liver to take it up ;fatty meal;second dose of Sestamibi@peak exercise scan is done 60 minutes later
🗑
|
||||
| Sestamibi collects where? | ischemic areas such as an MI;anything that is ischemic will have increased Sestamibi
🗑
|
||||
| patient who is having Sestamibi Protocol | hold caffeine or persantine for 12 hours prior to the test; hold your calcium channel blockers and your beta blockers for 24 hours if the patient is getting Persantine.
🗑
|
||||
| patient is getting Persantine | hold your calcium channel blockers and your beta blockers for 24 hours when having sestambi protocol
🗑
|
||||
| pulmonary artery catheter does are these 4 things,;. | measures pressure in different areas of the heart;measure cardiac pressure;infuse drugs with this catheter some catheters can even pace.;
🗑
|
||||
| Swan/Ganz catheter | pulmonary artery catheter; also called hemodynamic monitoring catheter
🗑
|
||||
| proximal port of swan gantz used for? | infuse fluids. You can use it for blousing, for cardiac output.
🗑
|
||||
| distal lumen of S/G (Pulmonary artery cath) | used to identify and measure pulmonary artery wedge pressure
🗑
|
||||
| thermistor on s/g (pulmonary artery cath) | used to evaluate cardiac output
🗑
|
||||
| balloon inflation port on S/G cath | where you inject the fluid for your cardiac output;
🗑
|
||||
| balloon inflation port on S/G cath for ? | balloon is used to help identify the pulmonary capillary wedge pressure or pulmonary artery wedge pressure
🗑
|
||||
| route of S/G balloon cath to measure pressure | catheter that is advanced through the right atrium down through the tricuspid valve into the right ventricle and then up to the pulmonary artery.
🗑
|
||||
| up into the pulmonary artery ; dicrotic notch here | shows closure of the the pulmonic valve
🗑
|
||||
| When you inflate the balloon in S/G cath | anything behind the balloon is obliterated. Cause this balloon can only see forward.
🗑
|
||||
| if the mitral valve is open in a S/G balloon look through cath then? | there is no obstruction between the tip of the balloon and the left ventricle and you can find out the left ventricular pressure
🗑
|
||||
| pulmonary artery catheter, you can | look at the right atrial pressure, the right ventricular pressure, the pulmonary artery pressure and the pulmonary artery wedge pressure which is giving you the left ventricular pressure
🗑
|
||||
| in SICU we never | wedge
🗑
|
||||
| dicrotic notch ; what does it mean? | closure of the pulmonic valve
🗑
|
||||
| arterial line or a hemodynamic monitor (S/G cath) you have to ? | level it; level it with the right atrium; called the phlebostatic axis.
🗑
|
||||
| phlebostatic axis is | 4th intercostals space of the right mid-axillary line
🗑
|
||||
| level the phlebostatic axis | take a carpenter’s level that is 6 foot long ; from the phlebostatic axis over to the transducer to level it.
🗑
|
||||
| transducer is too high | pressures are too low
🗑
|
||||
| transducer is too low | your pressure is too high.
🗑
|
||||
| phlebostatic axis location | 5cm below the angle of Louis)
🗑
|
||||
| complications of hemodynamic monitoring (swan/ gantz caths) | a pneumothorax can drop a lung when you put that swann in; patient goes for? A chest x-ry.Infection;dysrhythmias, foreign body in the heart Pulmonary artery ruptured/t overinflation of balloon > 1.5cc
🗑
|
||||
| inflate that balloon of the S/G cath with how much air | 1.5 cc of air, more can cause pulmonary artery rupture
🗑
|
||||
| what do you expect to see when you inject 1.5cc? | A change in the wave form;If it doesn’t change after that first injection, you should be a little concerned. don’t get a dampening of this wave form, then you are probably not in the right place.
🗑
|
||||
| How much do you need for an air embolism? | 5cc’s.
🗑
|
||||
| Normally, the CVP pressure is | anywhere from 0-8, that’s your right atrial pressure
🗑
|
||||
| what is your normal JVD? | <3cm. Add 5cm and you have your CVP.
🗑
|
||||
| right ventricular pressure | 20-30 for systolic and the diastolic is 0-8;
🗑
|
||||
| Pulmonary artery has a different pressure | systolic again of 20-30; more pressure there because of the valves and has a diastolic of 8-15
🗑
|
||||
| pulmonary artery wedge pressure | 8-12
🗑
|
||||
| cardiac output? | Stroke Volume X Heart Rate
🗑
|
||||
| can measure it with the hemodynamic monitor, or the Swan-Ganz, or the pulmonary artery monitor by injecting 10cc of saline in through the port, | draw back the 10cc and inject it at the end of expiration Quickly/ don’t inject it quickly,not an accurate reading.
🗑
|
||||
| computer calculates the time it takes for that 70 degrees of saline to change to 98.6 and that gives you your cardiac output. | Swan-Ganz measurement of CO
🗑
|
||||
| cardiac output comes from | left ventricle;
🗑
|
||||
| what causes a high PAWP? (pulmonary artery wedge pressure) | Too much fluid, too much volume, left ventricular failure
🗑
|
||||
| Increased afterload, what does that mean? Where is the pressure increasing – | in the aorta
🗑
|
||||
| warm up those blood vessels,what happens? | they no longer constrict they vasodilate.
🗑
|
||||
| What causes a decreased cardiac output? | Decreased preload
🗑
|
||||
| what causes decreased pressure in the right atrium – what causes pressure? | Dehydration; Sepsis.; Vasodilation,Increased volume ;ventricular failure; anaphylaxis; increased contraction of the heart
🗑
|
||||
| Why do you give Dig? | Slow the heart rate, but increase the force of contraction,
🗑
|
Review the information in the table. When you are ready to quiz yourself you can hide individual columns or the entire table. Then you can click on the empty cells to reveal the answer. Try to recall what will be displayed before clicking the empty cell.
To hide a column, click on the column name.
To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
To hide a column, click on the column name.
To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Created by:
goryan
Popular Nursing sets