NSG 3000 Exam 2 Guide

 About 50 questions are new content, 30 questions old content.

 Prioritizing nursing diagnoses: prioritize actual problems over risk for problems. This doesn’t
help with all ND questions. But when you are asked which ND is your priority, and 1 addresses
an actual problem while the other 3 address “Risks”, prioritize the actual problem.
 There is a heparin drip calculation on the exam. I will place a short supplemental video covering
this on Moodle.
 33% of the exam will cover respiratory, diabetes, HTN, CAD and MI.

Fluid and electrolytes GR and lecture (5 questions)

 Fluid Volume deficit/excess

o Excess:
 Cause: excessive intake, retention of fluid (HF, RF, SIADH), Cushing
syndrome, long term corticosteroids, or shift of fluid from interstitial to
plasma fluid
 Goal: remove fluid without producing abnormal changes in electrolyte
composition
 Treatment: diuretics and fluid restriction, restriction of sodium intake
 S/S: Headache, confusion, lethargy, Peripheral edema, JVD, Bounding
pulse, increased BP, Polyuria, Dyspnea, crackles, pulmonary edema,
Muscle spasms, Weight gain, Seizures, coma
o Deficit:
 Cause: loss of body fluid (diarrhea, fistula drainage, hemorrhage,
polyuria, overuse of diuretics), inadequate intake, third space fluid shift
(burns), shift of fluid from plasma into interstitial
 Compensation: of fluid out of interstitial in these patients will
cause nausea and vomiting
 Goal: replace water and electrolytes
 Treatment: balanced IV solutions (lactated ringers) isotonic solutions
(0.9% saline)
 Rehydrate these patients with isotonic solutions:
 0.9% saline, Lactated Ringers, D5W
 S/S: Restlessness, drowsiness, lethargy, confusion, Thirst, dry mucous
membranes, cold clammy skin, decreased skin turgor and capillary refill
postural hypotension, decrease urine output, concentrated urine,
weakness, dizziness, increased respiratory rate, weight loss, seizures,
coma
 Fluid imbalance (e.g. dehydration and overload)
o Critical assessment for these patients:
 daily weight
 intake and output
 serum BUN levels
 vital signs and pulse oximetry
  lungs sound
 skin turgor
 edema
o Dehydration:
 In a patient with dehydration r/t nausea and vomiting, they would have
a fluid shift from interstitial space to the blood vessels
 You would report a UO of 20 mL for 2 consecutive hours, because the
minimal UO for kidney function is 30mL/hour
 Early sing that dehydration has caused a fluid shift is restlessness, if
untreated leads to confusion and later coma
 To maintain hydration, run IV 75 mL/hour
 to rehydrate a pt, run IV 125 ml/hour (fluid bolus)
 monitor daily weights and intake and output
o overload:
 1 liter of water = 2.2 pounds
 Hyperkalemia/Hypokalemia
o Hyperkalemia:
 High serum potassium
 Causes: excessive potassium intake through potassium-containing salt
substitutes, the shift of potassium from the ICF to the ECF (metabolic
acidosis) or failure to eliminate potassium with kidney failure
 Causes a spiked T wave
 You are concerned with cardiac dysrhythmia (most life-threatening is V.
fib)
 It could result from hyperglycemia, renal insufficiency, or cell death,
excess protein from a blood transfusion, if the patient has nephropathy,
or from dehydration caused by high glucose
o Hypokalemia:
 Low serum potassium
 Causes: potassium losses through diarrhea, vomiting, diuresis, the shift
of potassium into the cells after insulin therapy, or lack of potassium in
the diet
 Causes a shallow T wave
 Treatment: IV or oral KCl, increased dietary intake of potassium
 Never push KCl
 For patients taking Digoxin, if they have hypokalemia, check for digoxin
toxicity
 S/S: weak irregular pulse, leg cramps (effects of loop diuretics)
 If a patient has hypokalemia: loop diuretics are contraindicated
 Hypercalcemia/Hypocalcemia
o Hypercalcemia:
 Causes: hyperparathyroidism or malignancies that cause bone
destruction
 S/S: fatigue, lethargy, weakness, confusion, bradycardia, and changes to
BP
 Teaching: weight bearing exercise keep calcium in the bones, pt should
increase daily fluid intake to 3000 to 4000 mL, complication could be
renal calculi
 o Hypocalcemia:
 Causes: primary or secondary hypoparathyroidism, renal insufficiency,
acute pancreatitis, malnutrition
 S/S: tetany (Chvostek’s sign, Trousseau’s sing), ECG changes (prolonged
QT interval)
 Pt with total thyroidectomy could have sign of Chvostek’s
 Treating hyperkalemia
o limiting foods high in potassium,
o administering IV insulin and glucose,
o administering IV calcium gluconate,
o changing to potassium-wasting diuretics (e.g., furosemide [Lasix]),
o hemodialysis,
o administering sodium polystyrene sulfonate (Kayexalate),
o IV fluid administration.
 You would not give potassium sparing diuretics like Spironolactone
(Aldactone)

ABG Lecture (3 questions)

 Alkalosis/Acidosis:
o Metabolic alkalosis: vomiting, nasogastric suction
o Respiratory alkalosis: hyperventilation
o Metabolic acidosis: diabetes
o Respiratory acidosis: respiratory failure
 ABG values:
o pH: 7.35-7.45
o CO2: 35-45  respiratory
o HCO3: 22-26  metabolic
o PaO2: 80-100
o O2 sat: >92%

Heart failure

 Primary risk factors: 1. Hypertension, 2. CAD

 Cause: diseases that affect CO (stroke volume [preload, afterload, contractility] and
heart rate)
o Preload- amount of blood returned to the heart, if you increase preload, you
increase the amount of blood that is returned to the heart (also known as End
diastolic ventricular pressure)
o Afterload- pressure against which the heart has to pump (the pressure in each
chamber of the heart has to increase in order to overcome systolic pressure)
(afterload is synonymous with blood pressure)
o Cardiac output- SV (amount of mL of blood ejected with each contraction) x HR
o Ejection fraction- percent of blood ejected with each contraction
 (stroke volume can go down with ejection fraction staying the same) (with
decreased preload, stroke volume is reduced, but this does not mean
ejection fraction goes down) (with decreased preload and normal ejection
fraction = end diastolic failing) (Decreased end diastolic filling)
  Normal ejection fraction: 55-60%
 Types:
o Left-sided:
 usually a result of systolic heart failure or diastolic heart failure
 Systolic heart failure– failure in pumping, it also has reduced
ejection fraction, usually caused by hypertrophy
o Cause: increased afterload (hypertension), impaired
contraction (MI), cardiomyopathy, valvular diseases
 Diastolic heart failure-- failure in filling, usually caused by
hyperplasia (which reduces size of overall chamber: decrease
afterload) “HF with normal EF”  decreased stroke volume and
CO
o Cause: L V hypertrophy (hypertension), MI, valvular
disease, cardiomyopathy
o Common: woman, older adults, obesity
 We treat both of these the same
 Risk factors: hypertension and MI (if you kill the cardiac cell with
infarction, then it is a weaker heart muscle- makes thinner wall, heart
failure is a complication of MI)
 S/S: pulmonary edema and congestion
o Right sided:
 Almost always a result of pulmonary hypertension (this can be
idiopathic, but people with COPD are more prone to it [risk factor]),
right sided heart failure is also known as cor pulmonale, pulmonary
embolism
 Symptoms: earliest – jugular venous distention [JVD], late symptom –
peripheral edema, others: hepatomegaly, splenomegaly, vascular
congestion of GI
 Compensatory mechanisms: SNS activation, neurohormonal (RAA system), dilation,
hypertrophy
 Compensation- all about blood pressure, maintaining appropriate blood
pressure, to get tissue perfusion (need MAP of at least 50 to get tissue
perfusion)
o Unstable- are they hemodynamically (heart and lungs) unstable
(something going on cardiac or respiratory)
 Decompensation- blood pressure dropping, now we are worried about shock
which is just poor tissue perfusion
o Tachycardia is the earliest sign of heart failure and shock (and of a
drop-in blood pressure)
o Decrease in blood pressure causes vasoconstriction which increases
afterload (we don’t want to see this – the decrease in BP was caused by
the increased afterload, the heart is now working too hard)
 Main medication for heart disease – Beta blocker (decreases sympathetic, which
decrease work of the heart)
 Acute decompensated Heart Failure:
o Failure of Left ventricle (2nd to CAD)
o Pulmonary vascular engorgement
o S/S:
  Pulmonary edema  anxious, pale, cyanotic, clammy, cold, dyspnea,
orthopnea, wheezing, coughing, crackles, increased HR, RR>30/min
 Chronic Heart Failure:
o Progressive worsening  ventricular remodeling
o S/S: fatigue, cough, dyspnea (PND- when patient is sleeping, suffocating feeling
because reabsorption of fluids), tachycardia, nocturia, skin changes, behavioral
changes, chest pain, weight changes
 Complications of HR: pleural effusion, dysrhythmias, L ventricular thrombosis,
hepatomegaly, renal failure
 Drug therapy:
o Diuretics: decrease fluid, preload, venous, edema [-ide, -zide, -zone, -one]
o Ace inhibitors: decrease fluid, improve bf, dilate, reverse modeling [-pril]
o ARBs: decrease fluid, improve bf, dilate, reverse modeling [-sartan]
o Vasodilator: decrease afterload, increase renal perfusion, decrease blood
pressure, preload, helps with dyspnea
o B-blockers: reverse remodeling, decrease afterload, inhibit SNS [-lol]
o + inotropes: [digoxin and dopamine] increase contractility, CO, HR, SV,
vasodilation
o Morphine: decrease anxiety, decrease preload and afterload
o Antidysrhythmic: prevent dysrhythmias
o Anticoagulants: prevent thromboembolism, good for pt with 20% EF or A fib
 Three Nursing Diagnosis associated with heart failure:
1. Decreased cardiac output
a. Signs/Symptoms:
i. Tachycardia
1. Give beta blocker (carvedilol- an alpha + beta blocker
[preferred choice for heart failure])
ii. Hypoxia
iii. Fatigue/SOB
1. Activity restriction
2. Positioning: Have them sitting up/give oxygen as ordered
iv. Hypotension (low blood pressure)
v. pallor, later- Cyanosis
vi. Decreased urinary output
vii. Decreased EF
viii. Decreased BP
ix. Decreased afterload
1. Give positive inotrope (digoxin)
x. +1 pulses
- Interventions:
o inotropic agent (dig, dobutamine)
o diuretic (furosemide)
o betablocker (carvedilol)
o oxygen
o activity restriction
o continuous heart monitor

2. Fluid volume overload

 a. Signs/Symptoms:
i. Weight gain
1. Daily weights
ii. Crackles
1. Give a diuretic – Lasix (furosemide) or Hydrochlorothiazide
or Aldactone
iii. Increased blood pressure (increased afterload)
iv. Edema (peripheral)
v. Fatigue
vi. Moist cough
vii. Bounding pulses
viii. Dyspnea
ix. Orthopnea (can’t breathe when flat)
x. SOB/tachypnea
xi. Increased preload
xii. Increased afterload
xiii. Increased BP
- Interventions:
o Strict I/O
o Fluid restriction
o Antihypertensive (ACE, carvedilol)
o Diuretic (furosemide)
o Oxygen
o Daily weight

3. Ineffective tissue perfusion

a. Signs/Symptoms:
i. Slower capillary refill (>3 seconds)
ii. Skin integrity tissues – chronic
iii. Skin changes (hair and shiny) - chronic
iv. pallor, later- Cyanosis
v. Decreased UO
vi. Fatigue/SOB
1. Activity restriction
2. Positioning: Have them sitting up/give oxygen as ordered
vii. +1 pulses
viii. Chest pain (draw troponin to check if they have MI) (usually less
than .01) (with a value of .03, this is a positive elevated value, which
means a weak heart)
1. Give a nitro [usually orally [isosorbide] or sublingual in these
cases]
2. Oxygen
- Interventions:
o Nitroglycerin
o Continuous heart monitor
o Activity restriction
o Oxygen
o Diuretic (furosemide)
 o d/c ACE if kidney function impaired (ACE is contraindicated in kidney
failure, impaired kidney patients)

Every one of these patients will have diuretic, oxygen, continuous heart monitoring

Need to know:

o coumadin is not for CAD but it is for A Fib

o warfarin prevents blood clots from forming in your heart
o A Fib promotes thrombus formation (increase risk of stroke), treat A Fib with
cardioversion, antidysrhythmic, anticoagulants, and “coumadin”
o ASA 81 mg daily is used to decreased CAD risk
o If patient is receiving coumadin daily it is for anticoagulation, for A Fib, or blood clot,
artificial, pacemaker, ICD
o Dyspnea with LVHF:
 Ineffective ventricular contractility
 Elevated pressure in the L atrium
 Fluid leaking to interstitial spaces
 Inadequate alveolar gas exchange
o Systolic HF has decreased CO and decreased EF
o Pulmonary edema from acute DHF, would be severe dyspnea and blood streaked frothy
sputum
o The left ventricle backs up into the pulmonary circulation
o Right sided HF shows as jugular distention, weight gain, peripheral edema, HR 108, and
tachycardia
o Preload is synonymous with volume
o HF patient is showing progress with Lasix if he is showing decreased preload
o Lasix (med for life) and Bumex are main drugs of treatment for HF patients
o To alleviate HF patient with anxiety and SOB, position in semi-fowlers, use relaxation
techniques, use calm reassuring manner, administer ordered morphine sulfate
o Morphine sulfate decreases anxiety and dyspnea
o Teach pt with exacerbation of HF to limit amount of milk and cheese, HF patients are on
a salt-restricted diet
o Teaching for nitroglycerin patch, avoid ED (erectile dysfunction) drugs
o Digitalis toxicity  anorexia and nausea, vomiting, blurred yellow vision, cardiac
dysrhythmias
o If they have a toxic dig level, have continuous cardiac monitoring and close watch
o Check potassium level for pt taking digoxin
o Pt with ADHF has severe dyspnea, you will first assist them to sitting position with arms
on bedside table [high folwers with feet horizontal or dangling]

Vascular

VTE (venous thromboembolism) Risk factors and treatment

- Thrombosis: VTE (DVT and PE)

 o Risk factors: caused by a clot forming in the vein d/t several factors
(cancer, sedentariness, lack of good blood flow through the veins,
surgery especially orthopedic surgeries) [surgery, injury, cancer,
sedentary]
 If there is calf thrombosis  unilateral swelling
 If there is a lung thrombosis  SOB, decreased O2 sat, chest
pain, increased RR
o You should ambulate our patients, and sequential pressure devices
(makes sure they won’t get a clot, give them heparin and lovenox
subQ (to prevent VTE), Eliquis  oral anticoagulant (risk factors for
these meds: bleeding)
o Unilateral leg swelling- report and doctor will get US of leg to check
for clot/dvt, will go home on apixaban, PE heparin drip, O2
o Lung: SOB, acute chest pain, increased RR, drop in O2; Leg: unilateral
swelling
o Prevent: heparin, coumadin, apixabans, treat symptoms

Venous stasis ulcer Treatment/chronic venous insufficiency/Risk factors and treatment

- Varicose veins & chronic venous insufficiency: lower extremity

o Veins have valves, pool in valves
o Chronic pressure on venous valves d/t fluid volume overload, obesity
or long periods of standing
 if it happens in the superficial veins: varicose veins
 In the deep veins: chronic venous insufficiency
 Risk factor: standing too long, chronic fluid volume overload,
HF, pregnant women
 Peripheral edema is a late symptom of HF, but if it is chronic
HF with peripheral edema, that is usually a result of valvular
insufficiency
o Assess: for varicose- stand up and look for bulging vein, for chronic –
look for edema in legs, swelling, browning and thickening of the skin,
venous stasis ulcers
 (impaired skin integrity biggest nursing diagnosis for this
swelling  because it can cause browning of skin and
thickening of the skin) the chronic also get venous stasis ulcers
(which are shallow ulcers you always find between the ankle
and calf, are seeping)
o Treatment: compression and elevation (do not need doctors’ orders
to do these two things or educate them on this) and UNNA boot
o Venous stasis ulcers will not heal unless you get rid of the edema, you
can put an ACE wrap around these ulcer legs (first wrap with
something to help with seeping: ABD)  this is not a tissue perfusion
problem
 o Don’t put pressure stocking on those with arterial diseases
o Chronic venous insufficiency – there is no surgery option for these,
we can apply curlex (dry dressing without a doctor’s orders)

PAD:

- Atherosclerosis: PAD (assume we are talking about atherosclerosis)

o No other cause of PAD except for atherosclerosis
o Plaque buildup in major arteries
o 50% of people with PAD had CAD -> most die of heart attack or stroke
o Risk factors for atherosclerosis: smoking, hypertension, obesity,
hyperlipidemia, high cholesterol, genetics, high fat diet, post-
menopausal women, male gender
o Assessment Symptoms: pain/claudication, cool extremities,
weak/decreased pulses (you can use doppler to still assess them),
pallor but dependent rubor (red extremities), decreased hair
growth/loss of hair on extremities, thinning of the skin, loss of
sensation/paresthesia, necrosis/arterial ulcers (distal ulcerations: toes
and heels)/gangrene, sequential BP, MRA, CTA, ABI: ankle/brachial
index
 Sequential blood pressures: patient lies supine, and get
brachial pressure and four cuffs around the legs, and look to
see where the pressure drop occurs (where the drop is will
show where the occlusion is in a noninvasive way)  we now
use MRA/CTA, can get a pictue of arterial bed, noninvasively
 if they go for these, there is dye, so we must know if they
are allergic to dye, and their kidney function (because these
patients will receive additional medications)
 Dye procedures: check for dye allergies, Iodine allergies,
Creatinine level, BUN shows their hydration level (if they are
dehydrated, give them IV)
 Claudication is specific for PAD, decreased blood flow to the
leg, they start to have pain when they walk and limp but is
relieved with rest (on test 2/3), it is reproducible pain
 Ankle/brachial index-- shows that what percentage of blood
flow is flowing through the ankle and arm, must be supine,
100% means no disease, if they are less than <0.8  they
must be seen for that
 Ankle pressure: 50, brachial: 100, 50/100 x 100  this
means you have 50% blood flow impairment in your
leg
 You can teach about what the percentage means, it is
in accordance to nursing practice
  If we want to prevent it from getting worse, and it
asymptomatic, treat the risk factors (smoking, HTN,
etc.)
 <0.7  start to have symptoms
 <0.3  this is considered acute ischemia
o Treatment: quit smoking, exercise (20 minutes walking is preferred)
[How do you teach them to start exercising when they have
claudication  they must walk through the pain  no stopping],
manage blood pressure, manage high cholesterol (med: statin [lowers
cholesterol]), lose weight, invasive: balloon angioplasty + stent (you
cannot stent in capillaries or arterioles, only in major arteries),
peripheral surgery bypass, prevent amputation, every patient who
has PAD should be on Clopidogrel (Plavix) an antiplatelet [super
aspirin]
 (because it prevents platelet aggregation: to prevent later
acute ischemia) (we tell these patients over 40 to take an
aspirin every day) (you can take both Clopidogrel (Plavix) and
the daily aspirin [no matter the dose] safely together)

ABI

 Ankle/brachial index-- shows that what percentage of blood flow is flowing through
the ankle and arm, must be supine, 100% means no disease, if they are less than
<0.8  they must be seen for that
 Ankle pressure: 50, brachial: 100, 50/100 x 100  this means you have 50%
blood flow impairment in your leg
 You can teach about what the percentage means, it is in accordance to
nursing practice
 If we want to prevent it from getting worse, and it asymptomatic, treat the
risk factors (smoking, HTN, etc.)
 <0.7  start to have symptoms
 <0.3  this is considered acute ischemia

Intermittent claudication Acute ischemia

- Claudication is specific for PAD, decreased blood flow to the leg, they start to
have pain when they walk and limp but is relieved with rest (on test 2/3), it is
reproducible pain
- Thrombosis: acute ischemia
 o Clot in major arteries
o Acute ischemia is more emergent than PAD
o Cause of acute ischemia: platelet aggregation injury, underlying
disease, underlying PAD, acute injury (to the lumen of the vessel)
o Assessment Symptoms: cold, severe acute pain, pallor, paresthesia,
paralysis, pulselessness [report these five symptoms: rush to surgery]
o Treatment: no lifestyle modifications  surgery is the only option
[angioplasty or bypass] (within 24 hours, hopefully within 12: because
there will be tissue death, losing toes)
 Anyone with PAD should be taking an antiplatelet
-

5 P’s
- The five P’s: pain, pallor, paresthesia, paralysis, pulselessness, poikilothermia

Vascular surgery (post op care)

Surgical considerations: come in with PAD or suspect acute ischemia
- Preop- must document the five P’s, main nursing diagnosis: acute/chronic
pain  must prioritize treating the pain  give opioids [morphine IV], for
impaired skin integrity (ulcer to the heel)- look at positioning – elevate heel
off of the bed, ineffective tissue perfusion- help by positioning them, in
chair with feet dependent, do preop teaching: teach them about what to
expect with the surgery [angioplasty: no general anesthesia]
- Postop- must document the five P’s, key after arterial surgery  look for
pulses, leg that has be revascularized  will be red and a little swollen due
to tissue perfusion, (with bypass there will be multiple incisions  fem to
fem bypass (look at the groin for the incision), fem post-tib bypass (incision
at fem and behind knee), you get them up post op day 1 for most bypass,
but for femoral bypass  recline them, no sitting up, balloon angioplasty
you can get them up immediately, monitor BP: if low, impaired perfusion of
bypass, if high, it will open sutures

- Vasospasm: Reynaud’s
o More often in women
o Predisposed from cold environment (exposure to cold)
o Occurs in small capillaries typically in the hand
o It does not stay in this state long enough to turn black
o Vasospasm of the capillary beds in the hands
o Assessment symptoms: hands, pain, pallor
o Treatment: wear gloves/protective clothing, avoid cold
(winter/freezer), avoid triggers, Med: CCB (prevent vasospasms)

- Inflammation: Beurger’s
o Acute inflammation in small capillaries
 o More often in men
o Predisposed by smoking  this does not go away until you stop
smoking
o This one will slough off tissue, kill tissue
o Assessment symptoms: pain, necrosis, gangrene, any extremity
o Treatment: quit smoking

- Phlebitis: inflammation of a superficial vein

o Occurs with poor IV care
o Red, painful that goes up the vein
o Poor PIV care
o Assess: IV for pain and redness, erythema
Arterial: PAD, acute ischemia, Reynaud’s, beurgers
- the classic symptom of lower extremity PAD is intermittent claudication
o The skin on the affected limb becomes thin shiny taut and hair loss
occurs on lower legs.
o Pulses are diminished or absent
o pallor develops in response to leg elevation, as blood cannot get to the
area distal to the plaque.
o Yet when the limb is in a dependent position, hyperemia develops.
o Finally, critical limb ischemia is when there is chronic ischemic rest
pain lasting more than 2 weeks, arterial leg ulcers, or gangrene of the
leg as a result of PAD.
- In acute arterial ischemia, arterial blood flow suddenly ceases. Tissue death
occurs, and if this tissue is a vital organ, it can be fatal.
o Commonly, the ischemia occurs when a thrombus is embolized,
traveling through the body until it lodges in a smaller artery (often
in the lower extremities). Most thrombus originate from the heart
- [aneurysm] Is a permanent, localized outpouching or dilation of the vessel
wall.
- [dissection] is the creation of a false lumen between the intima and media of
an arterial wall.
Venous: phlebitis, VTE, varicose veins, chronic venous insufficiency
- [Venous thrombosis] is the formation of a thrombus in a vein, and is also
associated with inflammation of this same vein.
- [Superficial vein thrombosis] is when the thrombus forms in a superficial vein
- [Deep vein thrombosis (DVT)] is when the thrombus forms in a deep vein
- [Venous thromboembolism (VTE)] is the term used to describe the pathology
for any deep venous thrombosis (from DVT to PE)
o Three main factors contribute to the development of venous
thrombosis in a limb. These three factors are called Virchow's
triad. Here are the components:
 [Endothelial damage] - damaged tissue stimulates platelet
activation and the beginning of the coagulation cascade
 (and thus creates a predisposition to developing a
thrombus).
 [Hypercoagulability of blood] - occurs in many disorders;
increases the likelihood of developing clots more than the
average person
 [Venous stasis] - dysfunctional valves or inactive muscles
leads to this
Write out the clinical manifestations (signs and symptoms)
of a VTE:

- edema
- pain/tenderness
- warm skin
- erythema/redness
- sense of fullness
- paresthesias
- dilated superficial veins
- slight temperature over 100.4
- duplex ultrasound.
- Based on the dose, some of these medications can also be used to prevent VTE
in at-risk patients. When you give 5,000 units of Heparin in clinical (or 40mg
Fragmin) for example, you are most likely administering the prophylactic
dose, NOT a treatment dose.
o Heparin: Serious side effect – HIT (Heparin Induced
Thrombocytopenia),
o IV Heparin: What lab do you monitor? – aPTT,
o tPA: Class – thrombolytic,
o Lovenox: Class – Low molecular weight heparin,
o warfarin (Coumadin): Class – Vitamin K antagonists,
o warfarin (Coumadin): What lab do you monitor? – PT/INR,
o Heparin: Class – thrombin inhibitor,
o rivaroxaban (Xarelto): Class – Factor Xa inhibitor
- In chronic venous insufficiency there is long-term vascular abnormalities and
impaired blood flow. This can eventually lead to changes in the skin, venous
leg ulcers, and long-standing pain.
- On the left is a picture of a venous leg ulcer, on the right is a picture of
vascular browning (the skin of the lower leg becomes leathery with a
characteristic browning color from hemosiderin deposits).
- Need to know:
o Warmth and palpable cord over vein  venous thromboembolism
o If giving vitamin K, you must know the prothrombin time because it
what is affected by coumadin
 o VTE  diagnosed by duplex ultrasound
o If patient has phlebitis  Remove IV
o Daily enoxaparin is for preventing blood clots
o If patient is taking Cardizem for Raynaud’s phenomenon, it will show
improvement by improving finger perfusion
o Compression stockings are not for PAD (rest pain)
o Venous insufficiency  dry itchy flaky skin
o PAD assist to walk after surgery
o Lovenox leave air bubble
o Enoxaparin is low weight use for DVT ineffective is leg swelling

ARTERIAL VENOUS

PAIN Yes, severe pain No, no pain, or aching pain at EOD

EDEMA No Yes

ULCERS Distal, often become gangrenous Ankles/calf

SKIN CHANGES Pale, thinning, hairless, dependent Peau d’orange: Browning,

rubor thickening
#1 NURSING DIAGNOSIS Ineffective tissue perfusion Excessive fluid volume
Other: pain/risk for infection Other: impaired skin integrity/risk
for infection

BEST INTERVENTION Smoking cessation and exercise Activity, Compression/elevation

(walking)

Kidneys

Terms: e.g. dysuria, oliguria

- Dysuria- painful or difficult urination

- Anuria- no urination <100ml in 24 hr
- Stress incontinence- involuntary urination with increased pressure
- Frequency- increased incidence of urination
- Nocturia- frequent nighttime urination
- Hesitancy- delay or difficulty in urination
- Hematuria- blood in the urine
- Oliguria- 24 UO of 100-400 mL
Urine specimens (e.g. clean catch) Kidney stones

- Enema the night before, ask about iodine allergies – IVP

- Ask about iodine allergy – Computed tomography with contrast
- Ask to remove all metal objects. Implanted metal objects are a
contraindication for the test. – MRI
- An x-ray, no special prep – KUB
- blood specimen, no prep – BUN and creatinine
- 24-hour urine collection – creatinine clearance
- Clean catch urine specimen – urinalysis, culture and sensitivity

Extracorporeal shockwave lithotripsy

- -Lithotripsy: use of high-energy shock waves to fragment and disintegrate

kidney stones. Outcome for lithotripsy is based on stone size, stone location,
and stone composition.
- -Cystoscopy: cameras are inserted into the bladder; stones can be removed.
Also used in hematuria to visualize the bladder and site/cause of bleeding.

Labs (e.g. creatinine)

- Creatinine- More reliable than BUN as a determinant of renal function. Creatinine is end
product of muscle and protein metabolism and is released at a constant rate. Reference
interval: 0.6-1.3 mg/dL (53-115 μmol/L).
- BUN: 6-20
- BUN/Cr ratio: 12:1
- Uric acid: 2.3-6.6
- Sodium 135-145
- Potassium: 3.5-5
- Calcium: 8.6-10.2
- Phosphorus: 2.4-4.4
-

UTI:

Diagnosis: Urinary Tract Infection (UTI)

Patho: An infectious organism enters the lower urinary tract via the urethra and ascends
into the bladder. Typically, the urinary tract has defense mechanisms to prevent such
infections from occurring (such as normal voiding with complete bladder emptying, and
antibacterial characteristics of urine - acidic pH).
Etiology: Most commonly the gram-negative bacilli normally found in the GI tract (E. Coli)
 Based on the above information, and what you know comprises a good urinary system
assessment, state 3 clinical manifestations you would expect to assess, and 3 nursing
interventions you would expect to perform:

Clinical Manifestations: dysuria, frequent urination, urgency, hesitancy, post void dribbling,
and suprapubic discomfort or pressure. The urine may be discolored and/or cloudy.
In older adults, the only s/s of a UTI is often confusion. They frequently do NOT have fevers
with a UTI.
Treatment/Nsg Interventions:

 Antibiotics to treat the infection

 Medications to relieve the pain and discomfort caused by the UTI (a heating pad to
relieve suprapubic pain!).
 Urine characteristics (color, clarity, odor), I & O, monitor HR, BP, and temperature,
monitor pain/burning

As nurses, we always want to care for the immediate needs of the patient. However, we also
are thinking ahead to prevent any complications of the pathological process occurring in the
body.
There are 2 main complications of UTI's that you need to be aware
of - pyelonephritis and urosepsis.
Pyelonephritis is a severe upper urinary tract inflammation, caused when the organism
(bacterial, viral, fungal..) has ascended through the bladder and up into the kidney itself. In
addition to the s/s of a UTI, patients with pyelonephritis also have flank pain (CVA
tenderness), fever, and chills. These patients can have fevers for days, even with
improvement.
Nursing Interventions: You'll get a UA and a urine culture, and expect to see orders for a
CBC (monitoring white count) and even blood cultures (to see if the infection has spread
into the blood stream). Antibiotics are needed, as well as fluids (IV and PO), close
monitoring of I &O and vitals, monitor urine characteristics, administer NSAIDs for pain and
fever, and monitor for sepsis (remember, sepsis is NOT the same as an infection in the
blood).
Urosepsis: You'll cover sepsis senior year, but for now I want you to know that sepsis
is systemic inflammation, often caused by a bacterial or viral organisms. When named
urosepsis, the sepsis is caused by a urinary source (i.e. a UTI or pyelo). Urosepsis can be
fatal, so monitoring for this complication is crucial.

Nephrotic syndrome

Diagnosis: Nephrotic Syndrome

Patho: Due to a wide variety of causes, the glomerulus becomes excessively permeable to
plasma protein.
 Etiology: Various; includes infections, diabetes, allergens, neoplasms, medications (NSAIDS).
Table 45-9 lists all causes, but you do not need to memorize.
Based on the above information, and what you know comprises a good urinary system
assessment, state 3 clinical manifestations you would expect to assess, and 3 nursing
interventions you would expect to perform:

Clinical Manifestations:

 ascites
 anasarca
 hyperlipidemia (decreased serum proteins stimulates the liver to undergo lipoprotein
synthesis (as body is searching for way to get protein) --> hyperlipidemia)
 massive proteinuria
 hypoalbuminemia
 Fun fact: hypercoagulability is common, because the anticoagulant proteins are lost in
the urine)

Nursing Interventions: We'll focus on the ones that deal with the edema:

 daily weights
 accurate I & O
 grading of edema
 replace protein by diet (you can give IV albumin, but it's debated on if this really helps.
The best way to increase albumin levels is by diet, but it takes TIME)

excess fluid volume related to edema

meds: corticosteroids, lipid lowering (statins)

Also you'll want to monitor for infections (as the immune system is weakened).

BPH (benign prostatic hypertrophy) signs and symptoms AV fistula

 Bladder outlet obstruction - often in men this obstruction is an enlarged prostate. Any male
that is voided small amounts frequently should be bladder scanned to determine their post-
void residual (PVR).
 Surgical interventions (TURP) to help treat prostatic enlargement and/or urethral strictures if
the cause of the retention is an obstruction

• Arteriovenous Fistula- feel turbulence, there is a thrill, use bell because it’s a high-
pitched noise, assess access site: palpate & auscultate AVF, Check Distal pulses and
Circulation
Pre/Intra/Post renal causes of AKI

- Prerenal. Prerenal causes of AKI are factors external to the kidneys. These factors reduce
systemic circulation, causing a reduction in renal blood flow. The decrease in blood flow leads
to decreased glomerular perfusion and filtration of the kidneys. Although kidney tubular and
glomerular function is preserved, glomerular filtration is reduced as a result of decreased
perfusion. LOW CO, hypovolemia
- Intrarenal. Intrarenal causes of AKI (see Table 47-2) include conditions that cause direct
damage to the kidney tissue, result- ing in impaired nephron function. The damage from
intrarenal causes usually results from prolonged ischemia, nephrotoxins (e.g., aminoglycoside
antibiotics, contrast media), hemoglobin released from hemolyzed red blood cells (RBCs), or
myoglobin released from necrotic muscle cells. ATN
- Postrenal. Postrenal causes of AKI involve mechanical obstruction in the outflow of urine. As
the flow of urine is obstructed, urine refluxes into the renal pelvis, impairing kidney function.
The most common causes are benign prostatic hyper- plasia, prostate cancer, calculi, trauma,
and extrarenal tumors. Bilateral ureteral obstruction leads to hydronephrosis (kidney
dilation), increase in hydrostatic pressure, and tubular blockage, resulting in a progressive
decline in kidney function. Hyperplasia calculi
 A dissecting abdominal aortic aneurysm is a prerenal cause of AKI because it can
decrease renal artery perfusion and therefore the glomerular filtrate rate.
Remember how preload is almost synonymous with volume? The same is true
with prerenal causes of AKI - prerenal causes are almost always due to
a hypovolemic state. In a dissecting AAA, the patient is losing volume.
 Aminoglycoside antibiotic administration, a hemolytic blood transfusion
reaction, and post-streptococcal glomerulonephritis are all intrarenal causes of
AKI. This is because these items all cause direct damage to the kidney tissue.

Aminoglycosides
Aminoglycosides: “a mean-old-mycin”
- Mean: treat serious illnesses, significant side effects/toxicity issues
- Mycin: all end in -mycin or -micin
- Used for resistant infections: MRSA, VRE, MDR,
- Used for systemic infection: multi-lobed pneumonia leading to sepsis (not for ear infection or
UTI)
- Toxicity: these meds cause ototoxicity (causes ear damage)
o assess for hearing, balance, dizziness
- Toxicity: these meds also cause kidney damage
o assess creatinine lab, GFR
- Toxicity: these meds cause damage to cranial nerve 8 (ear nerve), and should not be given more
than every 8 hours

There are 3-4 questions about Heparin/Coumadin. This table helps compare/contrast them

Heparin Coumadin
Prevents clots from forming (does not break up
Prevents clots from forming (does not break up clots)
clots)
Lovenox is a viable alternative (low molecular weight
apixaban (Eliquis) is a viable alternative
heparin)
Works immediately Takes days to reach therapeutic level
Used short-term (days/weeks) Used long-term (may be lifelong)

Therapeutic level determined by PT/INR

Therapeutic level determined by PTT
Administered IV or SQ PO only

Absolutely contraindicated during pregnancy

May be given during pregnancy
No dietary restrictions Teach patient to avoid green leafy
vegetables...they decrease the efficacy of
coumadin
Can be taken concurrent with coumadin while waiting
for coumadin to reach therapeutic levels in body.

BUN for dehydration