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O2 transport C
nursing 212 PEs and DVTs, shock
| Question | Answer |
|---|---|
| clotting cascade: extrinsic pathway- where is there damage; the damage to the tissue outside the vessel causes the tissue thromboplastin to activate what; | to the tissue outside the vessel; factor x; |
| clotting cascade: extrinsic pathway- activated factor X causes prothrombin to turn into what; when prothrombin turns into thrombin that causes fibrinogen to turn into what; fibrin makes what factor; after factor XIII causes what to be made | thrombin; fibrin; XIII; a blood clot |
| clotting cascade: intrinsic pathway- there is damage to what; the damage to the blood vessels does what to factor X; activated factor x causes the same sequence of events as extrinsic or different | the blood vessels; it activates it; same |
| pulmonary embolus: is this fatal; what are s/s; when does the chest pain get worse; why would EKG show changes | yes; SOB, chest pain; when pt takes a deep breath; b/c of the increase of stress on the heart; |
| pulmonary embolus: common causes; | predisposing factors, abdominal surgery, bone cases, |
| pulmonary embolus: causes- predisposing factors: increased ___ can cause clots; septicemia causes what; what other DX increases risk; | immobility;a hypercoagulation state; DM, smoker, obesity; |
| pulmonary embolus: causes- predisposing factors: why are obese women at increased risk; what med can increase the risk; what diagnostic study can cause it; what age increases the risk; | b/c they have more estrogen; birth control- the estrogen; swan gauze cath; >40; |
| pulmonary embolus: causes- abdominal surgery: why does risk go up; | the abdomen is very vascular and the pt is very painful and they are reluctant to get up |
| pulmonary embolus: causes- bone causes: why does this cause it | area of the body is kept really immobile and the bone was just manipulated |
| pulmonary embolus: Dx- what do ABgs show; what will EKG reveal; why is there right ventricle strain; | low O2 later and resp alkalosis at first bc pt is trying to compensate; R ventricle strain; b/c the clot sits in the pulmonary artery; |
| pulmonary embolus: Dx- what does the D dimer test show; when is D dimer elevated; | that there is a lot of fibrin degeneration; when there are excessive blood clots; |
| pulmonary embolus: Dx- what does VQ scan show; in VQ scan what would it reveal in a PE; | perfusion and ventilation- if they are mismatched or not; there is more ventilation then perfusion |
| pulmonary embolus: Dx- what does spiral CT show; what pt cannot have the spiral CT; | # dimension of lung image and it finds clot; kidney pt; |
| pulmonary embolus: Dx- what is the common dx | spiral ct |
| pulmonary embolus: Dx- VQ scan- perfusion with out ventilation means what; ventilation without perfusion means what, what is normal VQ; | there is a mucous clot; there is a clot in the system; 0.8; |
| pulmonary embolus: interventions- what interventions relieve hypoxia; what extreme med is given; what is given IV; | limit activity, assist ADL, O2, increase HOB, intubate; thrombolyics- need to know the risk benefit ratio; heparin; |
| pulmonary embolus: interventions- how often does pt have to be on Coumadin; what is done surgically to prevent it in the future; the intracaval filter is aka; what does the IVC filter do; what other surgical thing is done | 4-6 months; intracaval filter; greenfield filter; sits in the inferior vena cava and prevent future clots; thrombectomy |
| pulmonary embolus: prevention- what should be elevated; what should be applied to legs; what meds are given; what venapucture should be avoided; what do we need to teach about if pt is on coumadin | legs; IPC and compressionstockings; heparin oral anticoagulation;venapucture of lower extremities; vit K |
| Shock: def; early shock to late shock eventually causes ____ damage; what are causes; | inadequate/hypoperfusion of tissue; organ damage; low blood flow, cardiac failure |
| Shock: barorecptors respond to what change in blood volume; chemoreceptors increase in what change in pH; | decreased vol with sympathetic stimulation; decrease in pH |
| Shock: juxtaglomerular receptors respond to what change in blood flow; | decreased blood flow |
| Shock: does osmolarity increase or decrease; what osmolarity increases is there an increase or decrease of ADH; where does fluid shift; why does fluid shift that way; | increase; increase ADH; from interstitial to vascular; d/t decreased hydrostatic pressure |
| stages of shock: initial- what metabolism occurs; when anaerobic metabolism is used what rises; what are subtle changes that we notice; | anaerobic metabolism; lactic acid levels; restless increased resp rate, BG levels elevate; |
| shock- initial stage compensatory mechanisms in thebody- SNS stimulates the release of what; release of catecholamine increases what in the heart; the release of neurohormones vasocontricts of vasodilates; the neurohormones shunt blood to where; | catecholamine; contractility; vasodilates; the vital organs; |
| shock- initial stage compensatory mechanisms in thebody- what happens to urine when aldosterone is released; what happens to HR; what happens to glucose level; | dec in urine output <30 ml/hr; it increases; it increases; |
| shock- initial stage - body can tolerate this state if fluid loss is < ___ ml; if there is a smalle fluid loss what is used for replacement; what should we monitor | 700 ml; saline; output |
| stages of shock: the later stages occur when we do not realize what | the pt is in shock |
| stages of shock: Progressive- what is imbalanced; what ABGs is happening; why metabolic acidosis; why resp acidosis; | the electrolytes; metabolic acidosis, resp acidosis; bc increase in lactic acid; pt increased rr |
| stages of shock: what happens to the heart rate; hyper or hypo tension; why is there an ileus; what does skin look like; why is there a change in LOC | it is irregular; hypotension; hypotension; bc the blood is shunted away; pallor and cool skin; body is not tolerating this acidotic state |
| stages of shock: refractory- there is irreversible what; there is impending what; what causes listlessness | cell/organ damage to kidneys and gut; death; decreased cerebral edema |
| shock types: what is the most common type | hypovolemic |
| shock types: hypovolemic- where is the volume loss; does pt need replacement immediately; what should the replacement be; what else should be used for replacement; what to assess; | intravacularly; yes; packed red blood cells; albumin, saline, lactated ringers; orthostatic BP, HR, tugor |
| shock types: cardiogenic shock- heart cannot pump enough to do what; | perfuse cells; |
| shock types: cardiogenic shock- how does AMI cause this; how does mitral valve regurgitation cause this; what rupture can cause this; | there is loss of functional heart muscle; with each contraction of systole the valve regurges and does not pump properly; ventricular septal rupture; |
| shock types: cardiogenic shock- how does cardiac tamponade cause this; | heart gets all that pressure and cannot contract well; |
| shock types: cardiogenic shock- meds are used to do what; what should be repaired; what is tx for tamponade | improve cardiac contractility and BP; balloon pump; drain the pericardial sac |
| shock types: cardiogenic shock- what should we do for HOB; what frequent assessment should be done; we is UO assessed; | up; LS, UO; if kidneys are not being perfused they are not producing urine; |
| Shock: septic/toxic- person at risk has . .. HR___; temp ____; RR ____; | >90 , temp >102F; RR >29 |
| Shock: septic/toxic- toxins affect the vessels resulting in what; | vasodilation and capillary leakage; |
| Shock: septic/toxic- initially- what is temp. what is BP; what is HR; what is ABGs; | Shock: septic/toxic- |
| Shock: septic/toxic- later: what is temp; what happens to LOC; what happens to UO | down; decreased; anuric |
| Shock: septic/toxic- tx- how is fluid replaced; what type of solution is used; what med for BP; what is CVP goal; what ABX and why | 20-30 ml/kg; isotonic; pressors; between 8-12; IV broad spectrum b/c culture will take awhile; |
| anaphylactic shock: what is released b/c of antigen/antibody reaction; the release of histamine causes what; causes; | histamine; vasodilation and capillary leakage; allergies, bees and latex; |
| anaphylactic shock: s/s- 1st what do we notice; 2nd what do we see; 3rd what do we see; | pruritis,edema, tingling; resp distress, cyanosis, wheeze; circ. collapse |
| anaphylactic shock: adverse reaction from ___ products can cause this; | blood reactions; |
| anaphylactic shock: Tx- what does med epinephrine do; what does Benadryl do; | causes bronchodilation and increased CO; it is an antihistamine, pepcid |
| anaphylactic shock: interventions- what do we teach; what needs to be quick | prevention- know what causes allergic reactions and stay away from them; assessment |
| neurogenic shock: what is lost due to spinal cord injury; what spinal cord injuries have this; what other things can cause this; what is lost; when SNS tone is lost what takes over; when PNS takes over does it vasodilate or constrict | SNS nerve tone; T5 or above; spinal anesthesia, opiod overdose; vasomotor tone; the PNS; dilate |
| neurogenic shock: what happens to BP; what happens to HR; | low; low; |
| neurogenic shock: tx- what do we give initially hoping that it will help; what do we want to do to the cord; what other meds to we give; why are high doses of steroids given; why do we immobilize | fluid; immobilize it; vasoconstrictors; to dec spinal cord edema; to prevent further injury |
| shock tx: above all what do we need to know; if pt is low on volume what is tx; what meds are given; what isdobutrex for; what is given to vasocontrict | vs; give volume; dopamine, dobutrex; contractility; neosynephrine, levophed |
| vasoactive meds: what is dopamine for; what is used for aV node block; what are the vasopressors; what are the vasodilators | general circulatory support; dig; dopamine, norepinephrine, phenylephrine, epinephrine, vasopressin; nitro, sodium nitroprusside, fenoldopam, hydralazine, nicardipine |
| vasoactive meds: what med improves renal circulation; | dopamine infusion; |
| shock: interventions- what should be monitored; what lab is serially doneon trauma pt; why is H&H done serially; why are kidney functions done; why is lactic acid done; | BP, LOC, I&O, wts with appropriate interventions; H&H; incase there is a hemorrhage we do not see; to be sure pt is perfusing properly; bc of acidosis; |
| IABP: how does it work; when it inflates it forces blood back up to where; | used on pt w/ cardiagenic shock, inflates with air and inserted for low left ventricle function, takes the work load off of the left ventricle and inflates during diastole; to perfuse left ventricle; |
| IABP: who needs it; what do we monitor; what is HOB; how often should pt be repositioned; | unstable pts with cardiogenic shock; VS and cardiac indices; no further then 30 degrees;q2hrs |
| IABP: what leg needs to be restrained; what needs to be checked Q1 hr; what needs to be monitored; what med is given and why | the cathed leg; distal pulses; insertion site; IV heparin or lovenox to prevent clotting or emboli |
| coagulation + fibrinolysis: when does plasminogen turn into plasmin; after plasmin what does it turn into; after fibrin clot is brokendown what happen; what happens when these products are broken down | at the thrombin phase of coagulation; fibrin clot breakdown; fibrin degradation products; they are excreted and that is the end of fibrinolysis |
| DIC: aka; is this a primary or secondary disorder; this occurs secondary to what; this is the thrombi of what; what is microcirculation | disseminated intravascular coagulation; secondary; septic shock, post birth delivery; microcirculation; the capillaries; |
| DIC: what to counteractive things occur; the clotting and bleeding causes what in the blood; what is ABGs; what happens to clotting factors; this leads to what if not treated; | clotting and bleeding; stasis of blood; met acidosis; aggregation; ischemia, necrosis, multiple organ failure |
| DIC: what is onset like; what happens to the clotting factors | bleeding from any site; they are all used up |
| DIC: excess thrombin does what 2 things; the clotting ins the microvascular and macrovascular causes what to platelets; excess clotting causes what; | clotting in micro and macrovascular and converts plasminogen to plasmin; thrombocytopenia; ischemia; |
| DIC: ischemia causes what to organs; excess thrombin causin converstion to plasmin does what; excess FDPs cause excess what; excess bleeding causes what; | impaired organ perfusion; fibrinolysis with excess FDPs; excess bleeding; shock, hypotension and increased vascular permeability |
| DIC: platelet consumption is caused by ___ depletion; what do platelets look like in the beginning; what is norm platelets; what platelet count determines thrombocytopenia; | coagulation factor depletion; <140,00; 250-400,000;<50,000 |
| DIC: s/s- what would we see in the IV site; what other bleeding s/s; | bleeding; petechia; |
| DIC: stimulation of the fibrinolysis- this causes decresed what; fibrinogen is used to make up what; what is there an increase of; | fibrinogen; clots; fibrin split products (FSP); |
| DIC: Dx- what does the D-dimer show; | degree of fibrinolysis; |
| DIC: Tx- what is treated; why is heparin used; what is replaced; what clotting factors are replaced; what else is replaced; what is given to stop bleeding; no uneccesary ___ draws; | underlying disease; to stop clotting; clotting factors; platelets, FFp, cryoprecipitate; RBCs; vit K; lab draws |
| aortic aneurysm: where can it occur; where does it occur most often; | anywhere along the aorta; just below the renal artery and but the ileac; |
| aortic aneurysm: what causes it; what happens to the aorta; | arteriosclerosis and HTN; it does not expand or contract like it should; ; |
| aortic aneurysm: shape- what is fusiform; what is saccular; what is dissecting; | spindle shaped; unilateral outpouching; split or tear in intimal surface with bleeding into newly formed cavity between the vessel layers; |
| aortic aneurysm: tx depends on what; | how big the aneurysm is; |
| aortic aneurysm: where does pt go post surgery; is pt on teley; why does bp need to be controlled; what is risk post surgery GI; what is risk renal; what is risk peripherally; | ICU; yes; not to high not to low; ileus; high risk for failure; toe issues |
| hypertensive crisis: what is BP; s/s besides HTN; why does HTN need to be brought down slowly; | DBP >120-130; encephalopathy, lethargic, diffuse HA, confused; so we don't want side effects; |
| hypertensive crisis: what can happen neurologically; what can happen to the heart; why is there an AMI; | hypertensive encephalopathy; angina or AMI; b/c increased workload; |
| hypertensive crisis: what happens to pulmonary; what happens to the kidneys; | edema and fluid backs up into the lungs; excessive pressure fluid backs up into the lungs |
| hypertensive crisis: aka; what is treated in the BP; how is MAP measured; what med is given; | acute malignant HTN; MAP; DBP+1/3 pulse pressure; nitroprusside or NTG or labetalol; |
| hypertensive crisis: nursing Tx- what should be monitored; what should be assessed; | BP or MAP, chest pain, UO, EKG, abnormal labs; neuros; |
| pheochromocytoma: def; what percentage is malignant; what is the clinical presentation; who is at risk; what is the classic triad; | a catecholamine producing tumor of the adrenal medulla; 10%; classic triad; <35 yo; severe bounding H/a, tachycardia, diaphoresis; |
| Arterial embolism: is it more or less serious then venous; what are s/s; what are the 2 types; | more; pain in region, pulselssin extremity, necrosis in extremity; acute embolism,arteriosclerosis |
| Arterial embolism: tx- why are anticoagulants given; why are thrombolutics given; why are antiplatelets given; | to stop clot growth; to lyse clots; to prevent patelets from sticking |
| Arterial embolism: what are surgically interventions; what does endarterectomy do; what else can be done to reroute; | endarterectomy and embolectomy percutaneous transluminal angioplasty; it pulls out the clot; bypass grafting around occlusion |
| Arterial embolism: what should be checked; what part of body needs to be watched; what is prevented; SBP should not dip below what | circ with postop VS; the distal extremity; prevent hypotension; 100; |
| mitral stenosis/insufficiany- it impedes blood flow through what; what chamber gets larger; why does l atrium get larger; since blood backs up into the lungs there is less blood left in where | the L ventricle; L atrium; bc blood backs up into the lungs; the L ventricle for circulation |
| s/s L heart problems: what will ejection fraction be; what other s/s; | low; SOB,weakness, fatigue, syst. murmur; |
| aortic stenosis: it is asymptomatic until what; what happens to L ventricle; what happens to the afterload; what happens to O2 demands; s/s of it; is there increased or decreased CO2 | the opening is reduced to 1/3 of its normal size; hypertrophy; increases; they are increased; angina, syncope, fatigue, weakness, SOB, CHF; decreased |
| aortic regurgitation: what happens; what happens to the L ventricle; what happens to CO2; s/s; | the aorta does not close well; it hypertrophies; it is decreased; tachycardia, SOB, angina, diastolic murmur |
| vavular disorders: mechanical replacement- lasts how long; pt needs what meds for life; with heart sounds you can hear what; at dental appointments what does pt need to take; | for life; anticoagulants; audible clicks and murmurs; ABx; |
| vavular disorders: cadaver replacement- how long does it last | 10-15yrs |
| PE: what is the 3 classic s/s; | dyspnea, chest pain, hemoptysis; |
| shock: charecterised by what 2 things; all types of shock require differing _____ but have the same _______; | decreased tissue perfusion, and impaired cellular metabolism; tx, physiologic response of the body' |
| cardopgenic shock: there is comprimised what; causes; all of this altimately decreases what to body; less oxygenation does what to tissue perfusion; what is HR' what is BP; | CO; MI, dysrhythmias, cardiomyopathy, structural probs; oxygenation; decreases it; up; down; |
| shock: what are the 3 stages; | compensatory, progressive, refractory; |
| shcok: compensatory stage- what does the body activate to try to overcome anaerobic metabolism; what is the first sign of it; why is there a decrease in BP; when BP is low what does the carotid and aortic bodies do; | compensatory mechanisms; decreased BP; bc decrease in CO and narrowing pulse pressure; release baroreceptors |
| shcok: compensatory stage- what do baroreceptors do; where is blood shunted bc of activaation of SNS; so decreased blood flow to where accurs; | activate the SNS; to vital organs, heart, and brain; in the kidneys, liver, GI |
| shcok: compensatory stage-decreased blood flow to the kidneys activates what; what does renin do; decrease blood flow to GI causes what; decreased blood flow to skin causes what; what shock will not be cool and clammy | Renin; vasoconstrict; impaired motility and slowign of peristalsis; pt to feel cool and clammy; septic shock |
| septic shock: this is what response; what usually causes this'; this is because the bodies response to __ is exhausted; | systemic inflammatory response; gran neg and pos bacteria; antigen'; |
| shcok: compensatory stage- decreased blood flow to the lungs causes what; | increaed physiologic dead space; |
| shcok: progressive stage- this begins when; what are the 2 distinguishing feautures of this stage; altered capillary permeability allows what to leak out of the vascular space ino the interstitial; | as the compensatory mecahnisms fail; continnued decreased cellular perfusion and leaky capillaries; protein and fluid |
| shcok: progressive stage- is there an increase or decrease circulatiing volume; is there and increase of decrease of systemic interstitial edema; what part of the body usually shows critical dysfunction; | decrease; increase; the lungs; |
| shcok: progressive stage- what does the mvoement of fluid do to the lungs; what happens when fluid moves to the alveoli; | bronchoconstriction, decreased in functional residual capicity and fluid moves the alveoli; edema there and decrease in surfactant production; |
| shcok: progressive stage- what happens to mental status in this stage; what happens to kindeys; where can bleedign occur with this | decreased LOc not enough perfusion to brain; renal tubular ischemia; ulcers from the stress; |
| shcok: refractory stage- what caused the capillary leakage; what constricts venulues or arterioles; what dilates venules or arterioles; is recovery likely in this stage | increase in lactic acid; venules; arterioles; no |
| shock: what type of fluid is used and why; | colloids- to expand voluem; |
| shcok care: cardiogenic- what needs to be restored; hypovolemic-goal; septic- what is goal; | blood volume; stop the loss of fluid; fluid replacement, aBX; |
| what shock has high mortality rate | all but septic the most |
| shcok: what is the tx for neurogenic; goal for anaphylactive | depends on the cause; prevention and remove cause |
Created by:
jmkettel
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