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HNUR2502 Exam 3 Focused Review (Chapters 34, 35, 36, 38, 39, 40), Exams of Nursing

Utah Valley University (UVU)Nursing

⦁ heart failure ⦁ causes ⦁ A common chronic health problem with acute episodes often causing hospitalization. Acute coronary disease and other structural or functional problems of the heart can lead to acute HF. ⦁ Caused by systemic HTN in most cases ⦁ Common causes and Risk factors for HF: ⦁ HTN, coronary artery disease, cardiomyopathy, substance abuse, valvular disease, congenital defects, cardiac infections and inflammations, dysrhythmias, DM, smoking/tobacco use, family history, obesity, severe lung disease, sleep apnea, hyperkinetic conditions (hyperthyroidism)

Typology: Exams

2022/2023

Available from 08/21/2023

Briantaller 🇺🇸

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•UTAH VALLEY UNIVERSITY

HNUR2502 Exam 3 Focused Review (Chapters

34, 35, 36, 38, 39, 40)

• heart failure

• causes

• A common chronic health problem with acute episodes

often causing hospitalization. Acute coronary disease

and other structural or functional problems of the heart

can lead to acute HF.

• Caused by systemic HTN in most cases

• Common causes and Risk factors for HF:

• HTN, coronary artery disease, cardiomyopathy,

substance abuse, valvular disease, congenital defects,

cardiac infections and inflammations, dysrhythmias,

DM, smoking/tobacco use, family history, obesity,

severe lung disease, sleep apnea, hyperkinetic

conditions (hyperthyroidism)

• left vs right

• Left sided heart (ventricular) failure includes HTN, coronary

artery disease, and valvular disease. Decreased tissue

perfusion from poor cardiac output and pulmonary

congestion from increased pressure in the pulmonary vessels

indicate left ventricular failure

• Formerly referred to as congestive HF; not all cases of

LVF involve fluid accumulation

• May be acute or chronic and mild to severe.

• Two types:

• Systolic: heart cannot contract forcefully

enough during systole to eject adequate

amounts of blood into the circulation

• Diastolic: left ventricle cannot relax adequately

during diastole- ventricle can not fill with

sufficient blood to ensure an adequate cardiac

output

• Right sided heart (ventricular) failure may be caused by left

ventricular failure, right ventricular MI, or pulmonary HTN

(cor pulmonale). The right ventricle cannot empty

completely. Increased volume and pressure develop in the

venous system and peripheral edema results.

• diagnosis

• Labs:

• Electrolytes - may occur from complications or diuretics

• Hgb and HCT - identify HF resulting from anemia

• BNP - used when dyspnea to r/o HF

• U/A - proteinuria/high specific gravity

• ABGs- respiratory acidosis

• B-type natriuretic peptide (BNP)

• is used for diagnosing HF (in particular, diastolic

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Download HNUR2502 Exam 3 Focused Review (Chapters 34, 35, 36, 38, 39, 40) and more Exams Nursing in PDF only on Docsity!

• UTAH VALLEY UNIVERSITY

H NUR2502 Exam 3 Focused Review (Chapters

- heart failure - causes - A common chronic health problem with acute episodes often causing hospitalization. Acute coronary disease and other structural or functional problems of the heart can lead to acute HF. - Caused by systemic HTN in most cases - Common causes and Risk factors for HF: - HTN, coronary artery disease, cardiomyopathy, substance abuse, valvular disease, congenital defects, cardiac infections and inflammations, dysrhythmias, DM, smoking/tobacco use, family history, obesity, severe lung disease, sleep apnea, hyperkinetic conditions (hyperthyroidism) - left vs right - Left sided heart (ventricular) failure includes HTN, coronary artery disease, and valvular disease. Decreased tissue perfusion from poor cardiac output and pulmonary congestion from increased pressure in the pulmonary vessels indicate left ventricular failure - Formerly referred to as congestive HF; not all cases of LVF involve fluid accumulation - May be acute or chronic and mild to severe. - Two types: - Systolic: heart cannot contract forcefully enough during systole to eject adequate amounts of blood into the circulation - Diastolic: left ventricle cannot relax adequately during diastole- ventricle can not fill with sufficient blood to ensure an adequate cardiac output - Right sided heart (ventricular) failure may be caused by left ventricular failure, right ventricular MI, or pulmonary HTN (cor pulmonale). The right ventricle cannot empty completely. Increased volume and pressure develop in the venous system and peripheral edema results. - diagnosis - Labs: - Electrolytes - may occur from complications or diuretics - Hgb and HCT - identify HF resulting from anemia - BNP - used when dyspnea to r/o HF - U/A - proteinuria/high specific gravity - ABGs- respiratory acidosis - B-type natriuretic peptide (BNP) - is used for diagnosing HF (in particular, diastolic

HF), in patients with acute dyspnea

Microalbuminuria
- An early indicator of decreased compliance of the heart and occurs before the BNP rises - CXR
“early warning detector” that lets HCP know that the heart is experiencing early signs of decreased compliance long before symptoms occur
Helpful in diagnosing left ventricular failure because the heart is enlarged, representing hypertrophy or dilation - Echocardiography
Best tool in diagnosing HF- ejection fraction between 50-70%
Cardiac valvular changes, pericardial effusion, chamber enlargement, and ventricular hypertrophy can be diagnosed with this noninvasive technique
Can also be used to determine ejection fraction
Hemodynamic Monitoring
PA catheter allows for assessment of cardiac function and fluid volume
PAP (positive airway pressure) /PAWP (pulmonary artery wedge pressure) elevated with L sided HF because volumes and pressures are increased in the left ventricle o s/s ● - Left HF:
Decreased cardiac output:
Fatigue, weakness, oliguria during the day (nocturia at night), angina, confusion, restlessness, dizziness, tachycardia, palpitations, pallor, weak peripheral pulses, cool extremities
Priority problems:
Impaired gas exchange r/t ventilation/perfusion imbalance
Decreased cardiac output r/t altered contractility, preload, and afterload
Fatigue/weakness r/t hypoxemia
Potential for pulmonary edema r/t L sided HF
Pulmonary congestion:
Hacking cough, worse at night, dyspnea/breathlessness, crackles or wheezes in lungs, frothy, pink-tinged sputum,

Promoting oxygenation and gas exchange:
- Ventilation assistance
- Monitor RR q 1-4 hr
- Auscultate breath sounds q 4-8hr
- Position in high Fowler’s if patient dyspneic
- Maintain oxygen sat of 90% - education
Activity schedule, indications of worsening or recurrent HF, drug therapy, nutrition therapy, advanced directives, energy management
MAWDS (medications, activity, weight, diet, symptoms)
Indications of worsening or recurrent HF
Rapid weight gain (3lbs in a week or 1-2 lbs overnight)
Decrease in exercise tolerance
Cold symptoms lasting more than 3-5 days
Excessive awakening at night to urinate
Development of dyspnea/angina at rest - Increased edema in feet, ankles, and **hands
MI** o s/s
substernal chest pain / pressure radiating to left arm
Pain / discomfort in jaw, back, shoulder, abdomen
Pain lasting 30 min +
N/V
Diaphoresis, dizziness, disorientation

Dyspnea, fatigue
Fear & anxiety
Dysrhythmias, palpitations
Epigastric distress
Feeling “short of breath”
- diagnosis: EKG
- treatment: MONA, heparin, beta blockers, ca+ channel blockers, nitro, - nursing interventions **- education
MONA**
Morphine, Oxygen, Nitroglycerin, Aspirin
Valvular disorders (mitral regurgitation, aortic stenosis, mitral stenosis, aortic regurgitation, mitral valve prolapse) causes, s/s, treatment, diagnosis, complications, nursing interventions
Mitral Stenosis:
Valve leaflets fuse and become stiff narrowing valve opening and preventing blood flow from the left atrium to left ventricle
Increases pressure in left atrium leading to R ventricular hypertrophy
Pulmonary congestion and R sided HF first
Later, left HF and reduced CO
S/S:
Mild usually asymptomatic
As narrows:
DOE, orthopnea, PND, palpitations, dry cough, hemoptysis, and further signs of right HF
Rumbing, diastolic murmur
Mitral Regurgitation (insufficiency)
Prevent mitral valve from closing completely during systole allowing backflow of blood into left atrium when left ventricle contracts
Left ventricular hypertrophy to compensate for increased volume and pressure
S/S:
Remain symptom free for decades
Atrial fibrillation
High-pitched systolic murmur at apex with radiation to left axilla
Mitral Valve Prolapse (MVP) “clicks”
Valvular leaflets enlarge and prolapse into left atrium during systole
Marfan syndrome (tall man- “abe lincoln is the MVP”) and familial tendency
S/S:
Most asymptomatic
May have CP, palpitations, exercise intolerance
Midsystolic click and late systolic murmur at apex of heart
Aortic Stenosis:
Most common cardiac valve dysfunction in US
Aortic valve opening narrows and obstructs left ventricle outflow during systole

Management post-op pain, incision care, infection prevention
Mechanical valves require anticoagulation lifelong (goal 3-4 INR)
Care Coordination and Transition Management
Home care - may require home health nurse
Self-care:
Possibility of HR, drug therapy, prophylactic abx use, activity plan for rest
Teaching related to Vit K when on Coumadin (Warfarin)
Can usually return to normal activity after 6 weeks, but no heavy lifting with arms for 3-6 months
Wallet card, ID bracelet - Pulmonary edema
Life-threatening event that can result from severe HF (with fluid overload), acute MI, mitral valve disease, and possibly dysrhythmias
The L ventricle fails to eject sufficient blood, and pressure increases in the lungs as a result. The increased pressure causes fluid to leak across the pulmonary capillaries and into the lung airways and tissues
S/S:
Tx:
Crackles, dyspnea at rest, disorientation or acute confusion (especially in older adults as early symptom), tachycardia, HTN or hypotension, reduced urinary output, cough with frothy, pink-tinged sputum, premature ventricular contractions and other dysrhythmias, anxiety, restlessness, lethargy
Diuretics: Furosemide or Bumetanide
Morphine: if patients BP is adequate
In severe cases of fluid overload and renal dysfunction or diuretic resistances, ultrafiltration may be used
Ultrafiltration can remove up to 500mL/hr and uses a blood flow rate of 10-40mL/hr
Decrease in cardiac filling pressures, decrease in pulmonary arterial pressure, increase in cardiac index, reduction in norepinephrine, rennin, and aldosterone - Infective endocarditis
Microbial infection involving the endocardium - causes/risk factors:
IV drug abusers
Valve replacement recipients
Systemic infections
Structural cardiac defects: blood may flow from a high pressure area to a low pressure area eroding a section of the endocardium
HIGH MORTALITY RATE

s/s: Fever, murmur, heart failure (most common complication), arterial embolization, splenic infarction, neurological changes, petechiae, splinter hemorrhages - diagnosis
- Positive blood cultures
- New regurgitant murmur
- Evidence of endocardial involvement by echocardiography - treatment
- Nonsurgical:
  - Antimicrobials
  - Activities balanced with adequate rest
- Surgical:
  - Removal of infected valve
  - Repair or removal of congenital shunts
  - Repair of injured valves and chordae tendineae
  - Draining of abscess in heart or elsewhere **- nursing interventions
Pericarditis**
Inflammation or alteration of pericardium (membranous sac that encloses the heart) - causes
Acute pericarditis is most commonly associated with:
Infective organisms (bacteria, viruses, or fungi, usually respiratory)
Post-myocardial infarction syndrome (Dressler’s syndrome)
Postpericardiotomy syndrome
Acute exacerbations of systemic connective tissue disease - s/s
Substernal precordial pain
Radiating to left side of neck, shoulder, or back
Grating, oppressive pain, aggravated by breathing, coughing, swallowing
Pain worsened by supine position; relieved by sitting up and leaning forward
Pericardial friction rub
May have elevated WBC and fever - treatment
NSAIDs for pain
Corticosteroid therapy - pts who do not have bacterial pericarditis
Colchicine 0.5 mg orally twice a day for 3 months has been shown to prevent pericarditis recurrence
Bacterial pericarditis (acute) usually requires antibiotics and pericardial drainage
Chronic pericarditis may be caused by malignant disease my need radiation or chemo
Uremic pericarditis is treated by hemodialysis
The definitive treatment for chronic constrictive pericarditis is surgical excision of the pericardium - pericardiectomy - nursing interventions

Decreased HR, dyspnea, and fatigue
Muffled heart sounds
Hypotension
Cardiac tamponade is an emergency
Manage the decreased CO with increased fluid volume administration while awaiting an echocardiogram or x-ray to confirm the diagnosis
Tests are not always helpful because the fluid volume around the heart may be too small to visualize
Hemodynamic monitoring in a specialized critical care unit usually demonstrates compression of the heart, with all pressures (right atrial, pulmonary artery, and wedge) being similar and elevated (plateau pressures)
Pericardiocentesis: removes fluid and relieve the pressure on the heart
Pressures should return to normal as the fluid compressing the heart is removed and the s/s of tamponade should resolve - Cardiomyopathy
Disease of the heart muscle that makes it harder for your heart to pump out blood to the rest of your body
Can lead to HF - types:
dilated: most common, both ventricles dilated, systolic function impaired, decreased cardiac output
hypertrophic: ventricular hypertrophy, diastolic filling abnormalities, (athletes who die suddenly)
restrictive: rare, stiff ventricles that restrict filling during diastole
Tx like HF
arrhythmogenic right ventricular - s/s:
dilated: fatigue, weakness, LSHF, heart block, dysrhythmias, systemic or PE,s3/s4 gallops, cardiomegaly
hypertrophic non-obstructed: dyspnea, angina, fatigue, syncope, palpitations, cardiomegaly, s4 gallop, ventricular dysrhythmias, sudden death, HF
hypertrophic obstructed: (same as non-obstructed) + mitral regurgitation murmur, aFib **- diagnosis
treatment**
dilated: tx symp. HF, vasodilators, control dysrhythmias, heart transplant
hypertrophic: tx symptoms, beta blockers, aFib conversion, ventriculomyotomy w. mitral valve replacement **- nursing interventions
Heart transplants
nursing interventions**
immunosuppressants, s/s rejection, potential for tamponade - education

rejection: SOB, fatigue, weight gain (fluid), abdominal bloating, new bradycardia, hypoTN, aFib or atrial flutter, decreased activity tolerance, decreased ejection fraction (late sign) **- Hype rtensi on
causes**
Primary: family hx, Af. Am, hyperlipidemia, smoking, > 60 y/o, postmenopausal, excessive Na+ or caffeine intake, obese, overweight, physical inactivity, excessive alcohol intake, LOW potassium- mg+ - Ca+ intake, stress
Secondary: kidney disease, primary aldosteronism, pheochromocytoma, cushing’s disease, coarctation of the aorta, brain tumors, encephalitis, pregnancy, drugs (estrogen -OCs, glucocorticoids, mineralocorticoids)
s/s: typically no symptoms
h/a, facial flushing, dizziness, fainting - treatment
lifestyle modifications
drug therapy: diuretics (spironolactone, furosemide, hydrochlorothiazide), calcium channel blockers (verapamil), beta blockers (metoprolol), ACE inhibitors (lisinopril, enalapril, captopril), ARBs (losartan)
vasodilation decreases BP **- nursing interventions
complications**
target organ damage
HTN crisis (BP > 180/120)
give O
admin IV antiHTN (nitroprusside, nicardipine, fenoldopam, labetalol)
high fowler’s
IV NS slowly
monitor BP Q5-15m until diastolic <90, then monitor Q30m - education
fruits, veggies, whole grains, low fat diet
limit sweets, sugar beverages, red meats
low sodium < 2400 mg/day
aerobic physical activity 3-4x week for 40 minutes each
decrease modifiable risk factors
Atherosclerosis: plaque formation w/i arterial wall- leading risk factor for CVD - s/s
extremity cool to touch w. diminished pulse & cap refill
bruits in large arteries
elevated lipids, cholesterol, triglycerides
^ LDL, decreased HDL
diagnosis: cholesterol screening + hx
treatment: lifestyle changes - modifiable risk factors (smoking, weight mgmt, exercise)
diet to reduce LDL levels

Education:
- Walk until the point of pain, then stop and rest, and then walk a little more
- Avoid crossing legs or restrictive garments
- Maintain a warm environment with insulated socks
- Avoid cold, stress, caffeine, and nicotine which can lead to vasoconstriction **- Deep vein thrombos is
c a u s e**
smoking, HTN, certain diseases resulting to scraping along the blood vessels thus a platelet plug is formed
A blood clot that has formed in the lower legs like the calf or below the knee - s/s
calf/groin tenderness or pain
unilateral leg swelling
localized edema **- CPR
treatment**
rest + preventative measures
treatment goal: revolves along preventing dislodgement of clot → PE
D- don't walk or move too fast (bed rest), no hot pads, only warm & moist, no leg massage
V- venous return, elevate extremity
T- teaching DVT prevention:

Calf exercise
Hydration
Ambulation
No long sitting (car, airplane, bedrest)
Ted (tight knee length socks) & SCDs (sequential compression device) after clot has resolved
During clot:
Thrombectomy - removal of clot
Fibrinolytics
After clot: ●
anticoagulants
thrombectomy, ligation or external clips **- complications
Abdominal aortic aneurysm
s/s**
usually asymptomatic at first
gnawing pain that is unaffected by movement, can last for hours or days
pain in abdomen, flank, back
pulsating abdominal mass
diagnosis: xray (eggshell), CT for size & location, aortic arteriography, u/s, - treatment
maintain BP to avoid rupture
Abdominal aortic aneurysm resection
Thoracic aortic aneurysm repair
Endovascular repair **- nursing interventions
complications**
rupture > hypovolemic shock
hypoTN, diaphoresis, decreased LOC, oliguria, loss of pulses distal to rupture, dysrhythmias
Aortic dissection: blood enters aortic wall r/t sudden tear in aortic intima - s/s
pain- ripping, stabbing, tearing - treatment
eliminate pain, reduce BP, decrease velocity of left ventricular ejection - nursing interventions
Sickle cell disease: chronic anemia, pain, disability, organ damage, increased risk for infection, & early death r/t poor perfusion - S/S
decreased perfusion distal from occlusion leading to skin cool to touch & decreased cap refill, reduced or absent pulses
pain
fatigue, weakness, SOB
pallor, cyanosis
jaundice (RBC reduction = bilirubin release)

organ damage > death
priapism > anuria - education
causes of sickling: dehydration, hypoxia, infection
autosomal recessive trait
prevent crisis:
drink 3-4L fluids daily
avoid alcohol, tobacco
avoid extremes in temperatures (too hot / too cold)
avoid traveling to high altitude locations
genetic counseling
avoid strenuous physical activities
mild, low impact exercise >= 3 times weekly when not in crisis
Polycythemia vera: viscous blood w/ ^ RBCs- cancer - causes
massive production of RBCs
excessive leukocyte production
excessive platelet production - s/s
facial skin: plethoric (flushed), cyanotic or purple, distended veins
intense itching
HTN (r/t slowwwww moving blood & ^ heart demands)
Polycythemia vera, a condition in which too many RBCs are produced in the

blood serum, can lead to an increase in the hematocrit and hypervolemia,

hyperviscosity, and hypertension. Subsequently, the client can experience

dizziness, tinnitus, visual disturbances, headaches, or a feeling of fullness in

the head. The client may also experience cardiovascular symptoms such as

heart failure (shortness of breath and orthopnea) and increased clotting

time or symptoms of an increased uric acid level such as painful swollen

joints (usually the big toe). Hearing loss and weight loss are not

manifestations associated with polycythemia vera.

- treatment - apheresis (withdrawal whole blood, remove RBCs, plasma reinfused) - increase hydration - promote venous return - prevents clot formation - anticoagulants **- nursing interventions

complications**
- thrombosis r/t vascular stasis > tissue hypoxia, anoxia, infarction & necrosis
  - heart, spleen, kidneys - education
- 3L fluids daily
- avoid tight, restrictive clothing
- contact HCP at 1st sign of infection
- take anticoagulants as prescribed

support hose or stockings when awake & up
elevate feet when seated
stop activity if chest pain occurs
bleeding precautions
- NO flossing
smoking cessation
Hereditary hemochromatosis : autosomal-recessive disorder of HFE = increased intestinal absorption of iron - s/s
abdominal pain
hepatomegaly
hyperglycemia
gradual darkening of the skin
LATE problems:
diabetes, liver cirrhosis, endocrine gland failure, heart disease, death - treatment
reduce overall iron load
phlebotomy & removal of 500 mL blood at a time
twice weekly at first
GOAL: reduce blood ferritin levels (9-50 mcg/L) - nursing interventions
education on genetic testing
Myelodysplastic syndrome: formation of abnormal cells in bone marrow > decrease in all blood cell types (pancytopenia) - s/s
anemia, neutropenia, thrombocytopenia - treatment
allogeneic HSCT
supportive care
blood transfusions, platelet transfusions
erythrocyte stimulating agents (ESA): eopoetin alfa, darbepoetin alfa - nursing interventions
“precancerous state” pt education
administer transfusions
Leukemia: uncontrolled production of immature WBCs in bone marrow > reduced production of normal blood cells - causes
risk factors: ionizing radiation exposures, chemicals & drugs, chemotherapy agents, genetic & immunity risk factors
incidence increases with age - s/s
excessive bleeding episodes
bruise easily, increased menstrual flow, nosebleeds, gums bleeding, rectal bleeding, hematuria
weakness, fatigue, anorexia, weight loss, fever
h/a, behavior changes, decreased alertness, increased somnolence

pt will die if another transplantation does not occur
graft vs host disease (GVHD): donated marrow immunocompromised cells attack the recipient's cells, tissues, & organs
usually affected: skin, eyes, GI tract, liver, genitalia, lungs, immune system, musculoskeletal system
Veno-occlusive disease (VOD): blockage of liver vessels through phlebitis & clotting
w/i first 30 days following transplant
s/s: jaundice, RUQ pain, ascites, weight gain, hepatomegaly - education
preventing infection
poor clotting times = bleeding risk **- Lymphoma
hodgkin’s**
peaks in teens/young adults, adults in 50s-60s, more so in men
Epstein-Barr virus, HIV possible causes
starts in single lymph node, Reed-Sternberg Cells
predictable spread from one lymph node/group to the next - non-hodgkin’s
ALL lymphoid cancers that do NOT have reed-sternberg cells
spreads in an unpredictable manner
possible causes: solid organ transplants, immunosuppressive drug tx, HIV - s/s
large, PAINLESS, lymph node(s)
drenching night sweats
unexpected weight loss
some pts have NO symptoms - treatment
very treatable & curable
external radiation for Hodgkin’s
sperm banking for young men
monoclonal antibodies
HSCT
chemotherapy combo tx - education
pancytopenia
risk for infection & bleeding
permanent sterility- sperm banking options
secondary cancer development- need for continual follow-up
Multiple myeloma: WBC cancer, plasma cell secretes antibodies, overtakes bone marrow, increases cancer cell growth
progressive bone destruction, bleeding issues, kidney failure, reduced immunity, death
chemotherapy, steroids, autologous stem cell transplant
Autoimmune thrombocytopenic purpura: platelet PRODUCTION is NORMAL, with a massive DECREASE in CIRCULATING plts (plt destruction >

platelet production)

causes: unknown, suspected viral infections
Diagnosis: low plts + ^ megakaryocytes in bone marrow - s/s
- 1st in skin + mucous membranes
  - large bruises, mucosal bleeding easily
  - petechial rash on arms, legs, upper chest, neck - treatment
- therapy for underlying conditions + protection from bleeding episodes
- IV anti-Rho - prevent destruction of antibody coated plts
- plt transfusions (when cts are <10,000)
- splenectomy (site of excessive plt destruction) - nursing interventions
- maintain safe env’t
  - monitor any bleeding closely
  - infection prevention
  - bleeding precautions - complications
- intracranial stroke (bleeding-induced)
  - assess LOC & neuro function
- poor clotting = bleeding risk - education - vaccinations: meningococcal, pneumococcal, Haemophilus influenzae
- increased risk for infection (protocols)
- follow up with HCP
Hemophilia: hereditary bleeding disorder (A- lacks factor VIII (8) & B- lacks factor IX (9)) - s/s
excessive bleeding
joint & muscle hemorrhage - disabling long term issues
bruise easily
diagnosis: PROLONGED aPTT, normal PT - treatment
regularly scheduled infusions of missing factor **- nursing interventions
education
Blood transfusions
nursing care before**
verify prescription with another RN, assess lab values
type of product, dose, transfusion time
assess pt vitals, output, skin color, hx of transfusion reaction
test donor & recipient for compatibility (good for 72 hrs)
central catheter or minimum 18 gauge needle
verify pt identity w/ another RN
name & number, blood compatibility, expiration time - du ri ng
check blood tubing - NEED a filter & ONLY normal saline
remain w/ pt for first 15-30 mins