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BC3 cardiac lecture
BC3 cardiac lecture 1/22/08
| Question | Answer |
|---|---|
| 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, |
Created by:
goryan
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