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2.3.2 BO2 transport

oxygen transport B

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;
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
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
Created by: jmkettel