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2.3.2 BO2 transport
oxygen transport B
| Question | Answer |
|---|---|
| Angina: it is the imbalance between what 2 things; what 2 things can cause angina | myocardial blood supply that the heart gets and oxygen demand on the heart muscle; decreased O2 supply, increased O2 demand |
| Angina: causes of decreased O2 supply; causes of increased O2 demand; why does hypovolemia cause angina; causes of increased O2 demand | anemia, COPD, hypovolemia, PNA, CA spasm, dysrhythmias, valve disorders, bc there is not enough circulating O2; HTN, hyperthermia, physical exertion, substance abuse, aortic stenosis, cardiomyopathy, tachycardia,emotional stress |
| coronary circulation: what are the 2 main arteries that feed our heart; what supplies the anterior 2/3 of septum, anterior and apical L ventricle; what supplies the L atrium and lateral-posterior L ventricle; | the R and L coronary arteries; the Left anterior descending artery; L. cicumflex; |
| Angina: what supplies R side of heart and inferior L ventricle AV node and bundle ofHIS in 90 of ppl; | the R coronary artery; |
| Acute coronary syndrome: what is the most common cause of MI; what makes angina unstable; what is acute coronary syndrome composed of; | from CAD- atherosclerosis and plaque rupture; when pain does not go away at rest; CAD, unstable angina, NSTEMI, STEMI |
| unstable angina: is pain relieved by rest; is there ischemia; why is there ischemia; is there cardiac markers; are there EKG changes; is it predictable; will it worsen; | no; yes; b/c O2 deficit in heart muscle; no; no; yes |
| NSTEMI: what does this stand for; def; are there cardiac enzymes; are there EKG changes; what are EKG changes; | non ST elevated MI; there is a partial occlusion and partial thickness damage; yes; yes; ST segment depression, T wave inversion possible; |
| STEMI: AKA; def; are there cardiac enzymes; are there changes in EKG; what are the changes in EKG; | ST elevated MI; complete occlusion and full thickness damage- all heart muscle is damaged; yes; yes; ST segment elevation; |
| Acute coronary syndrome: do we fully understand what causes plaque to rupture; | no; |
| what are atypical s/s of unstable angina, lack of o2 in women; | fatigue,SOB, indidestion, anxiety |
| MI: occurs because of sustained _; sustained necrosis cause what; 80% are secondary to the formation of what; is contraction impaired in ischemic area; degree of contractile function loss depends on what | ischemia; necrosis; thrombus; yes; size of infarcted area; |
| MI: cardiac cells can withstand ischemia for how long before they die; ischemia begins where in the heart muscle; if ischemia persists with tx how long does it take before the entire heart wall is necrose; | 20min; in the deepest layers; 4-6 hrs; |
| MI: infarctions are described by what; degree of __ circulation influences the degree of damage | area of damage; collateral |
| NSTEMI: what part of heart muscle is the only part that is damaged | the inner heart muscle; |
| STEMI: what part of heart muscle is damaged; | all heart muscle; |
| MI: what ruptures; the plaque deposit becomes unstable and as it falls apart the body initiates what response; in inflammatory response what in body arrives; what 2 drugs are given asap to stop platelet agration | the plaque; inflammatory; platelets; ASA and plavix |
| clinical s/s of ACS/MI: PAIN- if pain is relieved by rest what kind of angina is it; what is the pain described by; where is pain found; where is the atypical pain found | stable; heaviness, pressure, burning, tightness, unrelieved by rest; substernal, retrosternal, epigastric, may radiate; L arm and jaw |
| some may describe the epigastric pain as what | heart burn |
| clinical s/s of ACS/MI: what will skin be like; what are the SNS reactions; | cool, clammy, ashen; HR increased, vasoconstriction of BV, |
| clinical s/s of ACS/MI: CV manis- there is an initial elevation of HR and BP, but it can drop with decreased what; with shock is there an increase or decrease of perfusion to organs; are there abnormal ht sounds; | CO; decrease; yes s3 and s4 murmers; |
| why does decreased CO cause BP to decrease | b/c of cardiogenic shock |
| cardiogenic shock most common where; | in the left anterior descending MIS b/c this oxygenates the L ventricle |
| clinical s/s of ACS/MI: why is there N&V; why is there a fever; inflammatory response is shown in elevation of what lab value | RT pain vasovagal resonse, stress; b/c the inflammatory process caused by cell death; WBCs; |
| clinical s/s of ACS/MI: most MIs occur when in the day | in the early morning; |
| clinical s/s of ACS/MI: what is the SNS response; vasoconstriction causes what s/s in skin; why is there tachypnea; | anxiety, tachycardia, vasoconstriction; cool clammy mottled skin; due to plain and blood changes |
| pathophys of an MI: after there is long plaque growth overtime what ruptures; when plaque ruptures what in body comes to site due to inflammation; platelet aggregation creates what; | the plaque; platelets; a thrombus; |
| pathophys of an MI: (cont) a thrombus creates a partial or complete ___; with vessel occlusion heart has less ____; with less O2 to heart cells ___; what is the end result | occlusion; O2; become hypoxic and die; ischemia/infarction |
| new Q wave that appears on the EKG can signify what | a previous MI- can persist for a life time |
| Troponin: when do they rise after heart attack; when are the peak levels; how long can they last | 3-6 hours; 18-24 hours; 14 days |
| treatment for MI: what is the rule for nitro; | 0.3-0.4 mg every 5 min up to 3 total doses; |
| MI and EKG: a negative T wave indicates what; a positive T wave that is very high indicates wath; | ischemia of the total heart wall or in the exterior wall layers of the ventricular muscle; ischemia to the interior wall layers of the heart |
| MI and EKG: myocardial injury- what segment will be displaced with myocardial injury; ST depression indicates __; ST elevation indicates what | the ST segment; injury of subendocardial layers in heart muscle; a lesion of the total wall |
| MI and EKG: an MI causes what wave to deepen; why does the Q wave deepen | the Q wave; this is a result of absence of depolarization from the dead tissue |
| shock equals decreased perfusion to where | the organs |
| LABS: Cardiac Enzymes- elevation of these enzymes help differentiate the chest pain as either ____ or ____; in angina is there damage to the heart muscle; in an MI is there damage to the heart muscle; what are the cardiac enzymes made of; | angina- no elevation or MI; no; yes; protein from dying cells being released into the blood; |
| LABS: Troponin- this is the most specific indicator of what; this protein is released when; what is the only muscle in the body that produces troponin; when does it elevate; | an MI; from dying myocardium; heart muscle; |
| LABS: Troponin- when does it elevate in blood after MI; when is the peak after MI; what are the 2 types; | 2-4 hours; 10-12 hours; CKMB/CK ratio; |
| LABS: Troponin- CKMB/CK ratio- ck ratio is aka; what are these; when do these elevate; when do they peak; when do they return to base; | CPK; waste products; 6 hours after MI; 18 hours; 36 hours; |
| LABS: Troponin- CKMB/CK ratio- increase in CK = __ injury; what is the CK that is specific to the heart; the CK MB helps quantify what; | any muscle injury; the CK-MB: the amount of myocardial damage; |
| LABS: Troponin- CKMB/CK ratio- what is a subacute mi; what lab will not be present if pt waits 3-4 days before going to the ER | pain not severe enough to pt and they wait 3-4 days before going to the ER; the CK-MB |
| LABs for MI: what should we look for in the CBC; Pt/PTT; why should we look at clotting; why look at ABGs; | increased WBCs; clotting; pt will be on heparin drip; O2 status and acid base balance; |
| LABs for MI: why look at BNP; why is lipid profile looked at; why is HgA1C looked at; | s/s heart failure; pt risk factors; pt diabetic control |
| EKG changes in MI: t wave inversion indicates what; what does elevated ST indicate; if there is a q wave what does that mean; is Q wave seen in ER; why is Q wave not seen in ER | ischemia; injury to heart; there is an infarction; no; it develops over time - tissue is no longer viable |
| EKG changes in MI: ST segment elevation is acute or chronic injury; | acute; |
| most MIs happen where in heart ; | at the bottom of the heart |
| EKG changes in infaract: why is there a significant q wave when one did not exist before; why is there not a q wave in a NSTEMI; | the impulse traveling away from the positive wave b/c tissue is electrically dead; not a full thickness loss so not all electrical function is lost; |
| EKG changes in infaract: in NSTEMI will there be an ST depression; NSTEMI is a precursor to what; | yes; full thickness MI; |
| EKG changes in infaract: criteria- the depth of q wave should be __% the height of R wave; width of Q wave should be what; what happens to the R wave; | 25%; 0.04 sec; the height of it is diminished |
| complications of MI: what is the most common complication of an MI; what is the most life threatening dysrhythmia; how long is pt at risk for dysrhythmia after MI; | dysrhythmias; Vfib - starts in Vtach; 24 hours; |
| complications of MI: heart failure- this is caused by failure of what; when the pump fails there is decreased ___; s/s of heart failure; these s/s are s/s of fluid ___; is the heart failure acute or chronic; heart failure can cause what serious thing; | the pump; CO; SOB, restlessness, agitation, pulmonary edema, s3 and s4, JVD; overload; acute; cardiogenic shock |
| cardiogenic shock means what | the organs cannot be perfused properly and pt can die |
| complications of MI:dysrhythmias- are the dysrhythmias slow or fast; what MIs are these most common in | slow; anterior wall MI |
| complications of MI: cardiogenic shock- what drug can be used to treat this; what does dopamine do in low doses; what does it do in high doses; does it increase or decrease BP and CO; | dopamine; it increases renal perfusion; increases contractility and vasoconstriction; increase it; |
| Dopamine: | |
| complications of MI: cardiogenic shock- this is when the functional myocardial muscle mass decreases by > __%; in this shock what cannot be perfused; what is the mortality rate; | 40%; the organs; >70% is not revscularized |
| complications of MI: what does infaract extension or expansion mean; infaract extension occurs when; when is there infarct expansion; | tissue continues to die or weak tissue stretches; when there is impaired blood flow and ongoing injury causing increased necrosis; when the muscles thin and dilate |
| complications of MI: pericarditis- def; s's of this; | inflammation of tissue surrounding the heart; friction rub, compression, pain; |
| complications of MI: structural defects- in this scar tissue causes what; what valve has issues; why does valves have issues | heart muscle dysfunction; the mitral valve; there can be damage to the charea tendineae |
| MI: nursing Dx- what should be tx for acute pain; why is there the dx of ineffective cardiac tissue perfusion; why is there decreased cardiac output; | nitro and morphine; b/c of plumbing problems; b/c heart muscle cannot meet bodies demands |
| nitro relief: can it relieve GI pain; | yes; |
| after MI why can liver labs be elevated | bc there can be deficit O2 in the liver causing the labs to fluctuate |
| Nitro: | |
| MI- Collabarative Care: why is time so important; S/S ACS are RT what; ischemia and injury progress to what over time; | time equals heart muscle- damage evolves over hours and cells die over time; myocardial ischemia; infarction |
| MI- Collabarative Care: unstable Angina- there is a partially occluded __; are there cardiac enzymes; are there EKG changes; | thrombus; no; no; |
| MI- Collabarative Care: NSTEMI- is there injury; what happens to the t wave; are there positive enzymes; is there a platelet rich thrombus; what will eMS give pt imediately | yes; it is inverted; yes; yes; aspirin |
| MI- Collabarative Care: STEMI- if we don't intervene what does this lead to; is there ST elevation; conduction problems can cause what; | infarction; yes; life threatening dysrhythmias; |
| MI- Collabarative Care: what is ER goal for pt with chest pain/mi | restore blood flow, treat dysrhythmias, stabilize |
| heparin: why is it given IV drip; | b/c it is faster and it can be stopped faster than subq |
| know anticoagulants *** | |
| What happens if pt has chest pain but negative enzymes: if enzymes are not found what is done next; | pt will go to nuclear med to further assess; |
| isotope stress testing: what is injected; what are the 2 types of isotopes; the isotopes eval what; what does test show | nuclear isotope; tallium, myoview; the uptake of tracer into heart tissue to measure coronary blood flow at rest and with exercise; O2 perfusion and demand of the heart |
| isotope stress test: during exercise what do healthy coronary arteries do; are blocked arteries able to dilate with excerise; the unequal dilation between healthy and blocked arteries causes more blood to be delivered wehre; | they dilate; not as well; to the heart muscle supplied by the normal artery; |
| isotope stress testing: reduced blood flow to part of heart where artery is occluded causes what to starve; the starvation produced what s/s; the amount oftracer uptake helps differentiate what | muscle; chest discomfort, SOB; normal muscle which receives more tracer to the obstructed muscle |
| MONA: what does this stand for; what does morphine do; what does O2 do; what does nitro do; what does asa or Plavix do; what else is hung in hospital | morphine, oxygen, nitroglycerine, apirin/Plavix; dilate arteries and manages pain; ups O2 supply in the blood; dilates peripheral circulation and coronary arteries; platelet inhibitor; heparin drip |
| Nitro: what vital sign should be checked and why | BP- it can drop very fast |
| morphine: this drug is given when chest pain is unrelieved by what; what does this do to the BVs; the vasodilation does what to bod O2 demand; what does it do to heart contractility; what does it do to BP and HR | nitro; vasodilates; decreases it; decreases it; decreases it; |
| Nitroglycerin: when given IV it immededietely does what to vessels; this dilation does what; what are the side effects; | vasodilates; increases coronary blood flow and decreases angina pain; pt can become tolerant and hypotension can occur; |
| Aspirin/Plavix: these do what; it interrupts the process or building _-- | they prevent platelet aggregation; a stable clot in the artery |
| Herparin: does it lyse clots; this prevents further buildup of what | no; clots |
| Filbrinolytics: these do what; they are used when what is not available; how fast should it be used; what are the names of some | breals up fibrin mesh in clots and restores blood flow; if cath lab is not available; first 6 hours post mi; streptokinase, tpa, retaplase |
| Beta blockers and MI: they decrease what; who should not get these; why can't pt with shock use these | O2 demand, HR, BP, contractility, risk for reinfarction and vfib; pt in shock; bp too low not enough perfusion |
| ACE inhibiters in MI: these prevent what in heart failure; for long term use these can redeuce the risk for what | ventricular remodeling; post MI heart failure |
| antidysrhythmics for MI: why are these given; pt will have block or a fib why | number one risk factor from MI is dysrhythmics; b/c of changes in tissue |
| MI tx in hospital: pt will be on what floor; what labs are drawn q8hs; what will be prescribed; what ivs are in; why is pt on bedrest; why should they use commode instead of bedpan; | telemetry floor; serial cardiac enzymes; O2;2 IVs 18 gage; to decrease cardiac workload; bedpan can create more stress then commode |
| MI tx in hospital: what should diet be; why is diet light; what tests are done; | light diet small frequent feedings; b/c circulation is shunted to GI to digest food and that is hard on heart; Echocardiogram cath lab; |
| echocardiogram: what does it show | heart muscle and valve function; |
| cath lab: why is this done | it will remove thrombus andrevascularize |
| cardiac cath: this is done when what; this diagnosis what; what side of heart are caths most common in | enzymes are positive; coronary artery flow; left side |
| cardiac cath: left heart- this is combined with ____ to determine location and severity of blockages and LV function; what artery is accessed; what artery access is more at risk for bleeding; | angiography; groin or wrist; femoral artery; |
| cardiac cath: right heart- what vein is accessed | one in neck or groin to measure pressure in right side of heart and lungs; |
| cardiac cath: revacularization- what does PCI stand for; examples of PCI; | percutaneous coronary intervention; angioplasty,artrectomy, stents |
| cardiac cath: revascularization- def of angioplasty: def of arthectomy; what are stents | balloon inflation of the arteries; removal of plaque; they are coated with and secrete meds to prevent occlusion again push back wall of artery; |
| cardiac cath: revascularization- what are complications; why is Plavix important; def restenosis; | dissection, spasm,restenosis; prevents artery from clogging; artery closing back up |
| cardiac cath: nursing care- what to monitor at insertion site; where should be circulation be assessed; why should s/s of PE be monitored | bleeding, inflammation; in extremity used for access; the dislodged clot can go to the lungs; |
| cardiac cath: what are the advantages of PCI | alternative to high risk surgical intventions, local anesthesia, patient ambulatory 24 hours after procedure, hospital stay 1-3 days while CABG stay 4-6 days, pt can return to work in 5-7days while CABG is 6-8 weeks |
| CABG: when is it needed; what is done; | when there is a complete occlusion of vessel, diffuse multivessel disease,failed PCI, servere LV dysfunction, DM, complete occlusion; new vessel is placed from aorta or subclavian vein to area distal to the obstruction in coronary arteries; |
| CABG: def sternotomy; why is pt temp decreased; what is placed temporarily in chest; | 6-8 in cut right through the sternum; this keeps the cells more stable at a colder temp; pacer wires; |
| CABG: what is the favorite artery to use; how long is IMA patent; | IMA- it remains attached to subclavian artery and anostomose to cardiac artery; 90% after 10 years; |
| CABG: the bypass pump does not perfuse what organs very well; what are not inflated during the procedure; with lungs not inflating what could this cause; why should chest pain be monitored post procedure; | the kidneys; lungs; atelactesis; it could be r/t reclotting of the graft and sternal incision |
| CABG: why should I&O be monitored; | <30 ml hr means kidneys are not perfusing- check for edema; |
| therapeutic hypothermia after cardiac arrest: it is used to prevent what; what does it do to the cell membranes; first what is done; after resuscitation what is done; how soon after mi should it be done; | ischemic injury in patients resuscitated after vfib or pulseless v tach-arrest; it stabilizes them; resuscitate; 32-34deg c; w/in 4 hours; |
| therapeutic hypothermia after cardiac arrest: where does this take place; what prevents shivering; what are adverse effects; why is pt rewarmed gradually; | ICU; meds to relax muscles; arrhythmia, clotting, electrolyte, imbalances, infection; to prevent IICP; |
| therapeutic hypothermia after cardiac arrest: how is this neuroprotecting; oxgen deprivation causes what with cells; why do cels die; | from slowing of cellular metabolism; death; b/c that cannot make aTP; |
| Cardiac Output: what is the equation; this output equals how much fluid is moved in 1 ____; also measures how fast ___; def stroke volume; | SV x HR; cycle; the blood is cycleing- HR; amt of blood/contraction from LV, amount of blood in a cycle in one ht beat |
| Cardiac Output: preload- increase stretch increases ___; with more stretch and strength is the heart able to fill more of less; if the heart can fill more can it pump more or less | strength; more; moer |
| Cardiac Output: preload- does it increase is HR increases or decreases; why does exersice increase preload; when does it decrease | decreases; b/c it returns more blood to the heart; speed up of the heart, volume loss, overstretching |
| Contractility: def; what lyte is the on switch of the cell; what going into the cell causes increased contractility | ability of the heart muscle to contract; calcium; calcium; |
| cardiac output - Contractility: what does the SNS do to contractility; what hormone will cause calcium to go into the cell; what does k+ do to contractility; what b/p med decreases this and why; | increases it causing heart to pump harder and faster; epi; decreases; cal. channel blockers bc they block calcium from entering the cells and with out calcium the cells cannot function |
| cardiac output: afterload- this is what; what increases afterload; | the resistance that heart works against- the push back; HTN, contriction, excessive viscosity or volume, stenosis; |
| cardiac output: afterload- why does HTN increase this; how does stenosis cause this | if the vessels are small and tight the heart has to push harder to push blood through them; gives the heart more pressure to push against- so heart needs to get bigger |
| cardiac output: afterload- why does viscosity cause this | a lot of extra blood volume asking the heart to work harder |
| what effects the stroke volume | preload, contractility, and afterload |
| cardiac output: what goes through the afterload eventually comes back as what | preload |
| what lyte repolarizes or resets the cell | k+ |
| CO is aka ____ on the echo | ejection fraction |
| Heart rate: what in body plays a significant role in rate control; sympathetic ns does what to HR; the parasympathetic ns does what to heart; | autonomic nervouse system; it increases HR tells CV to pump faster, harder and vasoconstrict; decreases heart rate; |
| Heart rate: what nervous system is rest and digest; what nervous system is fight or flight | parasympathetic; sympathetic; |
| does contractility go up or down when heart is pumping harder | up |
| heart: what are s/s if Right coronary arteries are plugged; | JVD, increase BP initially, edema, more hydrostatic pressure- fluid in belly; |
| heart: Left anterior descending MI- where does fluid back un into; what are s/s; what are s/s pulmonary edema | the lungs; crackles, pulmonary edema; SOB, O2 down, HR up, CO2 up , anxious, gasping for air; |
| heart: is afterload increased or decreased if body blood vessels push against L ventricle; what is the most common cause or right sided heart failure; | increased; left sided heart failure; |
| what should be the most frequent assessment with left sided heart failure | lung assessment |
| post MI heart Failure: LEft HF- where does it occur; what serious thing can this cause; what are s/s; | usually anterior MI around the L ventricle; cardiogenic shock; lungs sounds, HR, BP, urine output, tissue perfusion; |
| post MI heart Failure: LEft HF- where does this usually occur; what are the s/s | the Right ventricle infarct; hypotension, JVD distention, peripheral edema, liver engorgement, ascites |
| post MI heart Failure: systolic failure- what is the problem; will the ejection fraction be low or high | the heart pump pushing blood forward- it cannot do it effectively; low |
| post MI heart Failure: Diastolic- what is the problem; | muscle does not relax and it is stiff; |
| hemodynamic monitoring: what is this; what is the direct methods; what is the derived way; | invasive and noninvasive methods to collect data CV function; HR, arterial or venous pressure; calculated cardiac index, MAP, SV; |
| hemodynamic monitoring: what does MAP stand for; | mean arterial pressure; |
| hemodynamic monitoring: arterial/venous pressure- what does this measure; the pressure in the vessel is converted into what; | pressure, flow, oxygenation in the CV system; an electrical wave form; |
| hemodynamic monitoring: Arterial pressure- what is done to prevent clots; this can eval what; what is more sig than individual readings | pressurized infusion to prevent clots; response to interventions- shows what meds are doing and what procedures are doing; trends |
| intra-arterial pressure monitoring: this is aka;def; | art line; indwelling arterial line that allows direct and continuous monitoring of systolic, diastolic and mean arterial pressure; |
| what is the true real and accurate BP; | arterial BP |
| intra-arterial pressure monitoring: this is an easy access for what; what is most common artery used; what is MAP def; | arterial blood samples; radial; avg art pressure throughout a cycle |
| intra-arterial pressure monitoring: the MAP depends on what; | CO and SVR; |
| intra-arterial pressure monitoring: how is pulse pressure calculated; how is MAP calculated; what is average MAP; what number indicates organs are at risk for MAP; ex: what is the MAP of 120/60 | from SBP-DBP; DBP+1/3 pulse pressure; 80 in CV; 50; MAP= 60+ 1/3 (120-60) = 80 |
| intra-arterial pressure monitoring: when is this needed; what are ex of hypotenisive states; what pt should not receive this | hypotensive states; hemorrhage, shock, hemodynamic instability, vasoactive meds, surgery,HTM crisis, dissecting AA, vent or severe acid base imbalance; PVD, limp ischemia, coagulation, infection |
| intra-arterial pressure monitoring: Allen's test- this is used to asses what; | circulation to hand before arterial line placement of ABG sampling; |
| intra-arterial pressure monitoring: allen's test- procdure- where is pressure applied; what should pt do while pressure is applied; after fist open and close where is pressure applied and where is pressure released; then what is assessed | to radial and ulnar arteries; the have to open and close fist serveral times til blanches; arterial, ulnar; recirculation |
| venous pressure monitoring: where is the central venous cath placed; what is the primary use of this; what does it measure; | with the distal end in the SVC as it empties into the R atrium; monitor fluid status; blood volume, venous return, and filling pressure in the R heart |
| venous pressure monitoring: how is CVP measured; what does increased CVP mean; what does decreased CVP mean; | at end of expiration, pt at 45 deg, 2-8 cm H20;elevated pressure in RV just prior to systole; decreased venous return to R heart; |
| venous pressure monitoring: increased CVP indicates what in body; decreased CVP indicates what in the body; what increases preload into heart inc CVP or dec CVP; what decreases preload | fluid overload, vasocntriction, tamponade, PE; hypovolemia, shock; increased; decreased CVP |
| venous pressure monitoring: what are nursing interventions for this | pt needs to be in same position every time |
| pulmonary artery pressure monitoring: what is the cath used for this; is this still common; the balloon tipped cath is inserted where; from the RA where does the cath go next; this allows what to be measured; what are complications | swan-ganz; no; the central vein and threaded into the RA; thru the RV and into the pulmonary artery; the pressure in the RA, pulmonary A, LV; friction, need to be in ice; |
| pulmonary artery pressure monitoring: the wedge pressure is aka; | the filling pressure of the left attrium |
| pulmonary artery pressure monitoring: in the swan ganz cath how does the balloon facilitate in its placement; when the balloon is wedged into the pulmonary artery it allows for the indirect measurement of what; | it wedges in a small pulmonary blood vessel; the left atrium; |
| complications of invasive monitoring: what are they; how can a hemorrhage occur; what can cause a distal artery occlusion | infection, hemorrhage, pulmonary infarction/distal artery occlusion, displacement; if wall of pulmonary artery is poked; if the art line is wrecked |
| care of pt undergoing hemodynamic monitoring: when should pressures be measured; why should pressure be maintained on flush solution; how is central line placement verified; monitor what; why do we not want clots | between breaths; to prevent clots; by xray before infusion; infection, infiltration, phlebitis; b/c bacteria could get in it |
| care of pt undergoing hemodynamic monitoring: what should be consistent with measuring pressures | the pt position |
| cardiac output: the output eguals how much fluid moves in what; | a cycle and how fast it is cycling; |
| stroke volume: what are the 3 things that determine it; | preload, contractility, afterload; |
| what determines heart rate | autonomic nervous system |
| preload: the more the heart muscle is stretched the stronger or weaker it will contract; will the heart pump more or less if it fills more; | stronger; pump more; |
| preload: increased- with heart fill more or less; will it pump more or less; will the heart rate be slower or faster; A slower HR allows more time for what; more blood return to the heart will cause the heart muscle to stretch more or less; | more; more; slower; time for increased blood return to heart; more |
| preload: decreased- does the heart fill more or less; does the heart pump more or less; is the HR faster or slower; with faster HR does this give heart more or less time to fill | less; less; faster; less |
| would blood loss cause increased or decreased preload; why is preload decreased | decreased; body is attempting to slow blood loss |
| contractility: this is the ability of the heart muscle cells to do what ; can the heart muscle contract at diff stregnths; can skeletal muscle contract at different strengths; the contractility strength depends on how much ____ enters the cell; | contract; yes; no; calcium; |
| contractility: increased- what increases it; what does adrenalin do to increase it; | hormones, sympathetic nervous system, meds; stimulate k+ to leave the cells so more ca++ can get in to stimulate contraction |
| contractility: decreased- what causes it to decrease; how does acidosis cause this; | extracellular k+, acidosis, CC blockers; IC k+ is displaced by h+ into the ECF; |
| afterload: this is the resistance the the heart works ___'; this is the push back the heart has as blood does what; | against; leaves the heart; |
| afterload: increased- what increases it; how does increased Hct or excessive lipids increase it; | increased Hct, stenosis of vessel, excessive lipids in blood, HTN, contricted BVs, too much fluid; heart cant push around thick blood as efficiently; |
| heart Rate: increased- what nervous system increases it; what will the heart do in response to the SNS; | SNS; pump harder, faster and vasoconstrict; |
| heart rate: decreased- what nervous system decreases it; what does the heart do in response of the PNS; | PNS; rest and digest, vagus nerve |
| afterload: decreased- what are meds that decrease afterload; | diuretics, ace inhibitors, arbs, CC blockers, alpha blockers, beta blockers, meds that reduce excessive lipds; |
| afterload: meds that decrease- how do diuretics reduce blood volume; how do ACE inhibitors and ARBS reduce blood volume; | they take some of the volume out of the system; the promote the excretion of Na+ and H2O- salt is not saved so H20 follows |
| afterload: meds that decrease- how do ACE inh vasodilate; how do ARBs vasodialate; | the prevent the formation of angiotensin II- helps so heart does not have to push hard; they block angiotensin receptors on the heart; |
| what is the most potent vasoconstrictor in the body | angiotensin II |
| afterload: meds that decrease- how do CC blockers vasodilate; does blocking of Ca+ increase or decrease constriction; how do alpha cells vasodilate | the block the entry of Ca into the vascular cell; decrease it; the block SNS effect on muscle; |
| afterload: meds that decrease- how do beta blockers vasodilate; what med has a more cardiac effect against the SNS alpha blockers or beta blockers; | they block SNS; beta blockers |
| afterload: meds that increase- what are meds that increase it; when are pressors used; what do pressors do | pressors; in pt with shock; they vasoconstrict |
| inotropic meds- what do they affect in the cardiac muscle; how does it control the contractility; ex of ions | the muscles contractility; by controlling how ions enter and leave the cell; Na, k, Ca |
| positive inotropics: what ion is increased; this increase in ca+ increases what in heart; what pt are these used for; | Ca+; contractility; ht failure an cardiogenic shock; |
| positive inotropics: name these meds; how does beta agonists increase contractility; name beta agonists | beta agonists, digitalis, phosphodiesterase, calcium sensitizers; stimulate fight or flight SNS; norepinephrine, epinephrine |
| positive inotropics: how does digitalis increase contractility; | increases intracellular Ca+ by inhibiting Na and K+ pump; |
| negative inotropics: what do these do to ca+; decreasing ca+ increases or decreases contractility; decreasing contractility increases or decreases the o2 demand and workload of the heart; name these meds; | decrease it; decreases it; decreases it; beta blockers, cc blockers, centrally acting sympatholytics |
| negative inotropics: how do beta blockers decrease calcium; how do CC blockers decrease calcium; how do centrally acting sympatholytics decrease ca+ | compete with epi and norepi for binding sites to block SNS; by limiting uptake of Ca by cell to decrease the force of contraction; blocks sns in brain |
| beta blockers are used for what pt; cc blockers are used for what pt; ex of centrally acting sympatholytic | HTN< MI, angina, arrhrythmias, heart failure; HTN, angina, arrhythmias; clonidine |
| chronotropic meds: how do these effect the heart rate; what maintains the heart rate; | by altering how ions flow into nerve cells that control the ht rate or rhythm; conduction system- SA node; |
| chronotropic meds: what does chrono mean; what ions do these meds impact; for arrhythmias which med is appropriate; | time; na, Ca, k; it depends on the type/cause of it |
| positive chronotropics: do these increase or decrease hr what are are they; how do beta anonists increase hr; | increase it; beta agonists; they activate beta receptors that increase SNS effects thus increasing HR; |
| negative chronotropics: do these increase or decrease HR; what are they; | decrease it; sodium channel blockers , betablockers, potassium channel blockers, calcium channel blockers, dig, electrolyte suppliments, adenosine, atropine; |
| negative chronotropics: how do sodium channel blockers decrease HR; how do beta blockers decrease hr; how to k+ channel blockers reduce the hr; what is an example of k+ blocker | they block abnormally fast Na channels that rapidly depolarize in non-nodal; they inhibit sns reducing the rate and conduction; block k+ channels to delay repolarization and increase refractory period; amiodarone |
| negative chronotropics: how do cc blockers decrease hr; what arrhythmias areadenosine used for; what arrhythmias is dig used for; | decrease calcium entry into the cell which decreases both rate and conduction; SVT reentry arrhythmias; AV node blocker for atrial arrhythmias; |
| what does atropine do to vagal activity | inhibits excessive vagal activation |
| what should serum cholecterol be; triglycerides; | 200 or less; <150 |
| HTP is defined as BP> __ | 140/90 |
| angina: when the coronary artery is occluded and contractility ceases the myocardial cells are deprived of what; the deprivation causes what; as anaerobic met. begins what accumulates | O2 and glucose; anerobic metabolism to begin b/c no O2 for aerobic metabolism; lactic acid; |
| angina: the increased lactic acid causes what to be irratated; the nerve fibers do what; | myocardial nerve fibers; transmit a pain message to cardiac nerves causes angina |
| what is most common complication of MIs | dysrhythmias |
| the complication of heart failure post mi is dependent on what | the severity and extent of the injury |
| when does pericarditis occur psot mi | on day 2-3 |
| systolic failure: this is from the hearts inability to do what; what cannot contract; what is the hallmark s/s; | pump; the ventricles; decreased EF; |
| what is norm EF | 55% |
| diastolic failure: this is an impaired ability for the ventricles to do what; what is EF; what happens to stroke volume; what is wrong with ventricles; this pressure backs blood up to where; common cause | relax and fill; normal if no systolic issues; decreases; they are stiff and there is alot of pressure; other parts of the body-venous system; result left ventricular hypertrophy from htn |
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jmkettel
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