NUS 111 Test #2 - Oxygenation and Perfusion Flashcards
this is mainly lung disease cause by bacterium called Mycobacteria
tuberculosis
this respiratory disease can spread to lymphatic and circulatory system which can take it to the brain and bones
TB
how is TB spread
airborne transmission
What precautions do we put in place for active TB patients?
Negative air pressure room
N95 respirator
Single room with closed door
Gown
how long does it take TB to show after exposure
2-10 weeks
once inhaled how does TB travel
down to alveoli and body ingests bacteria
a potentially fatal form of disseminated disease due to the hematogenous spread of tubercle bacilli to the lungs, and other organs
miliary TB
dry mask and they calcify and make disease dormant
ghon tubercle
you can get tb again from these particles
ghon tubercle
since it’s airborne transmission - how exactly is TB spread. what does a person do?
coughing, sneezing, laughing, singing, talking
waht are the risk factors for TB
foreign-born
suppressed immune system
homelessness, poverty level
minorities
advanced age
poor access to healthcare
multi drug resistant strains
subst abuse
infants and children exposed to high risk pts
traveling abroad
Comorbities
Malnutrition
Diabetes
Silicosis
Chronic Kidney disease
Gastric or Intestinal bypass Surgery
what puts healthcare workers at risk for TB
*** know this
Administration of aerosolized medications
Sputum-induction procedures, including suctioning and coughing procedures
Bronchoscopy
Intubations
what immunocomprmised individuals are at high risk for TB
Human immunodeficiency virus (HIV) infections
Malignancies: Head, neck, lung, hematologic
Long-term corticosteroid use
Immunosuppressive drug therapies
Organ transplantation
what are the comorbidities of TB
Malnutrition
Diabetes
Silicosis
Chronic kidney disease
Gastric or intestinal bypass surgery
gerontologic considerations for TB
have atypical manifestations in elderly
alter mental status
create unusual behavior - anorexia, weight loss
fever
the tuberculin skin test produces no reaction (loss of immunologic memory) or delayed reactivity for up to 1 week
clinical manifestations of TB
signs and symptoms of pulmonary TB are insidious
-low-grade fever, cough, night sweats, fatigue, weight loss.
- cough is nonproductive but progresses to be mucopurulent.
-Dyspnea, chest pain, and hemoptysis (bloody sputum) occur as the disease progresses.
how is TB diagnosed
complete history, physical examination, tuberculin skin test, chest x-ray, AFB smear, and sputum culture are used to diagnose TB
RN assessments for TB
- assess for asymptomatic vs symptomatic disease
- perform physical assessment: auscultating lungs, night sweats, sputum, living conditions, risk factors, assess for presentation : is it active or not
Most ppl exposed to TB are….
asymptomatic and exposing ppl bc they are unaware
how many ways is TB classified
6 classes
class 0 of TB
Class 0: No exposure; no infection
class 1 of TB
Class 1: Exposure; no evidence of infection
class 2 of TB
Class 2: Latent infection; no disease (e.g., positive PPD reaction but no clinical evidence of active TB)
class 3 of TB
Class 3: Disease; clinically active
class 4 of TB
Class 4: Disease; not clinically active
class 5 of TB
Class 5: Suspected disease; diagnosis pending
nursing interventions for TB re patient teaching (5 ways)
patient teaching:
1. how not to spread disease
2. set up airborne precautions
3. ensure adequate nutrition intake
4. have exposed family members get tested
5. monitor vitals, assess effective cough, may need suctioning
what are the meds will active TB be treated with –at least 4 medications
INH, rifampin, pyrazinamide, and ethambutol
Primary drug resistance re TB
Resistance to one of the first-line antituberculosis agents in people who have not had previous treatment
Secondary or acquired drug resistance re TB
Resistance to one or more antituberculosis agents in patients undergoing therapy
MDR re TB
Resistance to two agents, isoniazid (INH) and rifampin. The populations at greatest risk for MDR are those who are HIV positive, institutionalized, or homeless.
how many weeks is the TB initial phase treatment last
8 weeks
continuation therapy is what weeks - TB
18 or 31 weeks
what medications are used during the continuation phase of TB
INH and rifampin or INH and rifapentine,
how do you determine if initial phase treatment for TB was effective
assess sputum smears
what is prescribed with INH to prevent peripheral neuropathy
vitamin B6 (pyridoxine)
how many drugs can be used for multi drug resistent TB
up to 6 drugs
how long will the treatment be for multi drug resistent TB
6-12 weeks
who will receive prophylaxis treatment for TB
-Household family members of patients with active disease
-Patients with HIV infection who have a PPD test reaction with 5 mm+
-Patients with fibrotic lesions suggestive of old TB detected on a chest x-ray and a PPD reaction with 5 mm+
-Patients whose current PPD test results show a change from former test results, suggesting recent exposure to TB and possible infection (skin test converters)
-Users of IV/injection drugs who have PPD test results with 10 mm+
-Patients with high-risk comorbid conditions and a PPD result with 10 mm +
what foods should pt avoid if taking INH
foods that contain tyramine and histamine (tuna, aged cheese, red wine, soy sauce, yeast extracts)
what does INH prophylaxis treatment consist of
daily doses for 6 to 12 months
what lab work needs to be checked if pt is on INH prophylaxis
Liver enzymes, blood urea nitrogen (BUN), and creatinine levels are monitored monthly to detect changes in liver and kidney function
what is the TB skin test called
Mantoux test - screening test
how is the mantoux test red
-pt exposure not currently active TB
-pt needs to go back after 2 days
priority labs/diagnostics for TB
- smears of sputum
- chest xray
- mantoux test
- bacteriologic studies
- screening tools - interferon - gamma release assays (IGRAs)
waht are some collaborative goals for pts with TB
- stopping spread
- meals on empty stomach
- return normal pulmonary function
- complete resolution of disease
- absence of complications to food access
- conditions can reactive disease immune suppression malignancy, quit smoking
what does croup cause
swelling of larynx, trachea and large bronchi due to infiltration of WBC
what does the inflammation of croup lead to
mucus and noisy breathing
waht are risk factors for croup - 2
recent upper respiratory tract infection
younger than 6 years old
acute LTB (laryngotracheobronchitis)
signs/symptoms - 5
- caused by viral illness
- symptoms come on at night, usually middle of night
- hoarse voice
- is reaction to cold or something similar
- barking seal like cough
acute spasmodic croup
signs and symptoms - 6
- caused by allergens
- hereditary
- reflux/allergy
- like an allergic reaction only higher in respiratory system
- reaction to something within body
- responds well to allergy/reflux meds
clinical manifestations for croup
- upper airway obstruction due to swelling of larynx, trachea and bronchi
- stridor - inspiratory breathing
- seal like cough
- chest wall retractions
- any changes in mental status
know croup sounds——
https://www.youtube.com/watch?v=C1q6ATkMtm0
what are the RN assessments for croup - 8
- assess for inspiratory stridor, barking cough, hoarseness, tachycardia and tachypnea
- using assessory muscles
- fever
- irritable
- recent URTI
- auscultate lung sounds
- hydration
- diminished breath sounds at bottom of lungs or the bottom of lungs sound normal
waht are the nursing interventions for croup - 8
- facilitate airway clearance
- go outside in cold air to stop cough
- run hot shower and sit in room
- run humidifier
- maintain fluid balance
- decrease fear to stop fight or flight mode in child
- anti inflammatory meds
- give educ to parents about croup so they know what to look for
what are the labs/diagnostics for croup
observe clinical symptoms
meds for croup
dexamethasone: 0.15mg-0.6gm/kg orally
racemic epinephrine through neubulizer
safety measures for croup
- dont leave child alone
- maintain pt airway
- flu vaccine - type B for epiglottis
- Need to stay in hospital 4 hours after being administered racemic epinephrine
influenza virus affects respiratory tract how - 2 ways
- direct viral infections
- by damage from immune system response
this virus transmission occurs through a susceptible individuals contact with aerosols or inanimate objects can carry and spread disease and infectious agents from infected individual
influenza
this creates inability of lung to perform its primary function of gas exchange which can result from multiple mechanisms, including obstruction of airways, loss of alveolar structure
influenza
risk factors for influenza - 6
- unvaccinated individuals
- compromised immune systems
- young/elderly
- chronic medical conditions
- pregnant women
- residetns of long term care facility
what needs to b e considered when old person gets flu
- immune system declines as adults age
- prevent secondary infection
- flu increases risk of heart attack 3-5x and stroke 2-3x in first two weeks of infection in 65+
clinical manifestations for influenza
- fever
- chills
- hypoxia
- severe headaches
- D & V
- cough
- muscle aches
- fatigue
RN assessments for the flu
vital signs, normal assessment of chest auscultation, look for signs of dehydration
subjective/objective data of pt: around anyone that’s sick, feeling sob, dyspnea on exertion, lung sounds, RR, BP, pulse ox, accessory msucle use, etc
labs/diagnostics for flu
health history - clinical findings
flu A & B test
RSV test
COVID test
how long do flu cultures take to come back
how long do rapids take
3-10 days
15-60 mins
nursing interventions for flu
- droplet precautions
- lots of fluids
- relief of symptoms
- keep track of I & O if severe
- antipyretics - Tyle & Motr
- analgesics - tyle & motr
- rest
- gargle warm salt water
safety considerations for pts with flu
droplet precautions
infants, elderly, hc workers
guillain-barre
anaphylaxis hypersensitivity to eggs
most effective strategy for managing influenza is preventative admin which is….
influenza vaccine yearly
” the ability of blood to transport oxygen-containing hemoglobin to cells and return carbon dioxide-containing hemoglobin to the alveoli”
perfusion
priority meds for the flu - 3
need to look up more details in ATI 17, 20, 23
- zanamivir (inhaler)
- oseltamivir (tablet)
- peramivir (IV)
infection of the lower respiratory tract caused by a variety of microorganisms, including bacteria, viruses, fungi, protozoa, and parasites
pneumonia
what are classifications of pneumonia - 5
community-acquired pneumonia (CAP),
hospital-acquired (nosocomial) pneumonia (HAP),
ventilator-associated pneumonia (VAP),
health care–associated pneumonia (HCAP), and
pneumonia in an immunocompromised patient.
waht are the vectors pneumonia can arise from - 5
- from normal flora present in patients whose resistance has been altered;
- aspiration of flora present in the nasopharynx or oropharynx;
- the inhalation of airborne microorganisms from other persons (sneezing, coughing, or talking);
- contaminated water sources or respiratory equipment;
- blood-borne organisms that enter the pulmonary circulation (hematogenous spread) and become trapped in the pulmonary capillary beds
most common microbe in CAP
***know this
streptococcus pneumoniae
risk factors for pneumonia – all types
smoking
age
malnutrition
post surgery
large family/lots of kids
pulmonary edema (fluid in lungs)
altered level of consciousness
toxic inhalation
chronic condition/pre existing hypoxemia
risk factors for HAP/VAP
Debilitation
Malnutrition
Altered mental status
Previous exposure to antibiotics (within the last 90 days)
Hospital stays of 5 days or longer
High rates of antibiotic resistance (hospital or unit-specific)
Immunosuppressive therapies or diseases
Prolonged (greater than 48 hours) intubation or a tracheostomy
Male gender
risk factors for HCAP
Hospitalization for 2 or more days in the last 3 months
Chronic dialysis within the last month
Home wound care within 30 days
Recent home IV therapy (antibiotic, chemotherapy)
Resident of a skilled nursing or extended-care facility
Family member with drug-resistant microorganism
risk factors for immunocompomised pneumonia
chemo treatmetns
autoimmune disorders
corticosteroids
malnourished
broad spectrum antibiotics
old ppl considerations for pneumonia
get more detials from honan 303
can get missed due to not showing all signs of pneumonia
clinical manifestation for pneumonia
SOB
hypoxic
crackles and wheezes in lungs
fever
chest pain
productive cough
leukocytosis elevated (5000-10000 normal range)
fatigue
anorexia
tachypnea
SpO2 low
use secondary assessory muscles
RN assessments for pneumonia
-auscultate breath sounds
-monitor for complications
1. rate, depth, efforts of breath
2. sign of septic shock - low BP, tachycardia
3. use of accessory muscles
4. super infection
5. respiratory failure
6. thoracentesis
7. confusion
8. empyema
9. atelectasis
waht is a super infection and give example
overgrowth of good bacteria which then becomes bad
ex. c diff
what can septic shock lead to
multisystem organ failure
what is the leading cause of death for severe pneomina
respiratory failure
fever, dehydration, hypoxemia, sleep deprivation, or developing sepsis … can lead to this
confusion
collapsed alveoli.
it can improve with coughing and deep breathing
atelectasis
nursing interventions for pneumonia
-incentive spirometer
-vaccines
-who’s at risk for pneumonia - ID and prevent them from getting it
-physical assessment
-oxygen therapy, hydration, antibiotics, neubulizer
-teaching how to cough and deep breathing techniques
-re-evaluate lung sounds, pulse ox, RR
-ambulating and staying active
-positioning
chest percussions to help loosen sputum
pt teaching for pneumonia
-decrease the spread - stay home
-when to follow up with doctor
-take every dose of antibiotics
-know drug to drug interactions
-repeat chest xrays
-get vaccines
-cough can last for several weeks
labs/diagnostics for pneumonia
chest x ray
CBC - check WBC
arterial blood gas
meds that treat pneumonia - early onset (less than 5 days) with no risk of multi drug resistant pathogens
Ampicillin-sulbactam
OR
Ceftriaxone
OR
Levofloxacin, moxifloxacin, or ciprofloxacin
OR
ertapenem
meds that treat pneumonia - late onset (5+ days) with risk of multi drug resistant pathogens
Cefepime
OR
Imipenem or meropenem
OR
Piperacillin-tazobactam AND Ciprofloxacin or levofloxacin
OR
amikacin, gentamicin or tobramycin AND vancomycin (MRSA)
3 safety measures for pneumonia
- decreased perfusion/oxygenation
- any changes in cognition
- safety considerations based on meds they are given
this is the balance between clot formation and clot dissolution
hemostasis
balancing throughout the whole body
homeostasis
why does the body need clotting mechanisms
to prevent bleeding
what is fibrinolysis
clot dissolution
what is thrombus
clot formation
mini clots in atria which can become emboli and travel to the brain (stroke). top chambers of heart not opening properly
atrial fibrillation
caused by a thrombus that impairs blood flow. blood clots off artery causing heart not to work bc blood isnt getting to body properly
myocardial infarction
increases heart workload and contributes to atherosclerosis. heart is working harder, blood has smaller areas to go through
hypertension
what 3 things affects perfusion by alterations in hemostasis
- atrial fibrillation
- myocardial infarction
- hypertension
keeping a good balance is important btwn which two mechanisms
thrombus and fibrinolysis
what is normal BP
120/80
what is pre-htn bp
120-139/80-89
stage 1 htn bp:
140-159/90-99
stage 2 htn bp
160+/100+
HTN crisis bp
180/120
pathophysiology of HTN
thicker blood (viscosity) or small vessel radius =increase pressure
increase pressure (resistance) = higher BP
atherosclerosis (plaque) leads to narrowing of arteries
narrowing of the arteries leads to increase in BP
GOAL = manage resistance against what heart must pump
HTN is known as
the silent killer - you dont know you have it
high BP from an unidentifiable cause
primary HTN
higher BP from an identifiable cause
secondary HTN
if you stop medications abruptly, can have sudden increase of BP
rebound HTN
what’s it called when BP higher than 180/120, true emergency - will lead to organ damage
hypertensive crisis
modifiable risk factors HTN
-stress
-excessive dietary sodium
-sedentary lifestyle
-smoking
-alcohol
-drugs
-oral contraceptives
-diabetes type II
this creates water retention means more water in CV system so increasing pressure
excessive dietary sodium
nonmodifiable risk factors HTN
age
african american
family history
gender
this to consider for old ppl and HTN
HTN increases with age
age causes functional & structural changes in body
risk of polypharmacy
Na+ restriction
lifestyle modifications
include family in teaching
what are the symptoms of hypertension
HTN does not present with symptoms until its too late
hypertension can speed up what disease
coronary artery diease
what issues does hypertension create
organ damage, blurry vision, loss of vision, ischemia, pooling of blood
pts with HTN have a higher chance of getting what
stroke
what are the RN assessments for HTN
-monitor vital signs
-assess and reassess before and after giving BP medications
-CV and respiratory assessments
what does a nurse look for during CV and respiratory assessments when pt has hypertension
looking for chest pain quality and length
edema
lung sounds - may hear crackles
during HTN assessment - what does a nurse assess for signs of complications of (5)
- coronary artery disease (CAD)
- cerebrovascular disease
- peripheral vascular disease (VAD)
- nephrosclerosis
- retinal damage
labs and diagnostics for HTN
CBC - complete blood count
BMP - basic metabolic panel
Serum lipid profile
serum liver function studies
serum thryroid tests
12 lead EKG
history & physical exam findings
during a CBC for HTN - what do you specifically look at
platelets, RBC, WBC, hemoglobin, hematocrit
during BMP for HTN - what do you specifically look at
BUN, creatine, electrolytes (Na, K, Mg, Cl, glucose, CO2)
patient teaching for HTN
-low or normal fat - good v bad fats
-exercise
-no smoking/alcohol or other drugs
-decreasing stress
-high BP screenings
-screened for diabetes
-look for comorbid conditions - elevated lipids, diabetes, use alcohol or drugs
-teach signs and symptoms of distress so pt knows when to go to provider
meds for hypertension
- beta blockers
- ACE inhibitors
- diuretics
- anticoagulants
these are blood thinners
examples
anticoagulants
ex: heparin, warfarin, enoxaparin
lower BP by pulling off fluid resulting in diuresis
list 2 examples
diuretics
ex: furosemide, bumetanide
lower blood pressure. all drugs end in “pril”
examples
ACE inhibitors
ex: lisinopril, enalapril
lower heart rate and blood pressure. all drugs end in “lol”
examples
beta blockers
ex: metoprolol, atenolol
collaborative goals for pts with HTN
-lifestyle modifications
-avoid tobacco
-psychosocial
-diet change
-exercise
pathophysiology of PVD - peripheral vascular disease
-characterized by reduced blood flow through vessels
-peripheral arterial disease (PAD) comes under the umbrella of PVD.
-lumens narrow —> blood flow decreases —> tissue ischemia
unresolved tissue ischemia = ?
infarction
risk factors for PAD - peripheral arterial disease
atherosclerosis (CAD)
smoking
obesity
family history
age
race
Pre-existing health conditions:
Coronary artery disease
Cerebral artery disease
Diabetes
Hypertension
Dyslipidemia
Clotting disorders
Hyperhomocysteinemia
clinical manifestations for PAD
some pts are asymptomatic
unequal lower extremity pulses (or absence of pulses)
loss of hair on leg area
shiny appearance on area of the LE
arterial assessment for pts with PAD
Be alert for the following signs and symptoms, known as the “Six Ps”:
Pain (severe, shooting, stabbing, or burning sensation)
Pallor (lighter color than the rest of the skin)
Pulselessness (no palpable pulse)
Poikilothermia (cool temperature to palpation)
Paresthesia (numbness, tingling, hot/cold sensations)
Paralysis (immobility [late sign], indicates severe tissue damage)
what is intermittent claudication
pain may be described as aching or cramping in a muscle that occurs with the same degree of exercise or activity and is relieved with rest.
what is the hallmark symptom of PAD
intermittent claudication
what causes intermittent claudication
by the inability of the arterial system to provide adequate blood flow to the tissues in the face of increased demand for nutrients and oxygen during exercise
how is intermittent claudication relieved
Relieved by stopping muscle use
overall review of intermittent claudication
- Cramp-like pain in a muscle
- Consistently reproduced with the same degree of exercise or activity
- Relieved by stopping muscle use
- Caused by inability of the arterial system to provide blood flow that keeps up with increased demand
- Site of arterial disease can be determined by the location of claudication
- Pain occurs in muscle groups distal to the diseased vessel
- 70–80% of patients do not have worsening symptoms
- 10% of claudicants will progress to critical limb ischemia (CLI) (White, 2016)
- Dependent position reduces pain
during a focused assessment - waht do you look for for PAD
Structural changes, resulting from chronic lack of oxygen and nutrient delivery to the tissues:
Hair loss distal to the occlusion
Thick, opaque nails; shiny, dry skin
Skeletal muscle atrophy
Skin color changes:
Elevational pallor
Dependent rubor (red color when limb dependent from dilated damaged vessels)
Pulse changes:
Pulses diminished or absent below area of stenosis/obstruction-pedal, posterior tibial, popliteal, femoral
Cool extremity distal to occlusion
Sensation changes:
Paresthesias
Numbness
Tingling of extremities
Ulcers or gangrene
Edema
lab/diagnostics for PAD
-c-reactive protein (CRP) - inflammation marker
-homocysteine level
-serum lipid profile - triglycerides, HDL/LDL & Cholesterol
-doppler ultrasound - of the extremities
-ankle-brachial index
-angiography - locates extent of the PAD. Contrast dye injected which can confirm or refute arterial disease
surgical revascularization to improve blood supply from aorta into femoral artery and the vessels below the formal artery. incision made down the medial part of leg with PAD
arterial bypass
surgical procedure that may be performed with or without a stent. balloons inserted into vessel where might be plaque
angioplasty
post op nursing interventions for PAD
- check distal pulses
- assess incision site
- perform NV checks to leg (6 Ps)
- assess for signs/symptoms of compartment syndrome
- monitor for bleeding/thrombosis
- assess mental status (any signs for decreased perfusion)
- health promotion - assess for PAD risk factors
- avoid heating pads/heating blankets
- use compression socks/devices
- moist dressings
- control blood sugars
- assess any wounds for s/s of infection
what is the pt teaching that needs to happen post op regarding PAD
- wear socks, shoes
- keep feet dependent for maximum blood flow to LEs
- no bare feet
- diet modification - decrease high cholesterol foods, decrease saturated fats, less refined sugar, encourage vitamin c, proteins & zinc
meds for PAD
-analgesics for pain
-cilostazol (pletal) for intermittent claudication
-clopidogrel (plavix) for protection from platelet aggregation
-aspirin or other anticoagulants to keep blood thin
-medications to treat atherosclerosis:
*ACE inhibitors
*diuretics
collaborative goal for PAD - arterial
anticoagulant therapy (IV heparin then warfarin), surgical interventions - thrombectomy, fem/pop
collaborative goal for PAD - venous
- compression devices, dressing care, nutrition/diet
arterial ulcer:
location
location: Distal to arterial stenosis, heels, toes, over bony prominences, metatarsals, malleoli, between toes, trauma points
arterial ulcer: ulcer-base
Dry, pale gray or yellow; may be necrotic
arterial ulcer: shape
Border regular and well demarcated
arterial ulcer: surrounding tissue
Pale; cooler than other skin areas. In longstanding insufficiency, skin is thin.
arterial ulcer: edema
Minimal unless leg is dependent often
arterial ulcer: pain
Claudication. Rest pain; continuous pain worsens with elevation and eases with dependency.
arterial ulcer: pulses
May be absent or diminished; often disappears with exercise
venous ulcer: location
Around ankle, lower third of leg, more often on medial side
venous ulcer: ulcer-bas
Generally shallow but may be deep. Pink, but may be beefy red with granulation tissue. Ulcer bed usually moist. May have copious drainage
venous ulcer: shape
Irregular border
venous ulcer: surrounding tissue
Darkened color in gaiter area. Temperature higher than other skin areas. Brawny edema. Skin may be thick and fibrotic (woody). May be oozing and crusted
venous ulcer: edema
may be severe
venous ulcer: pain
Aching, throbbing, heaviness. Superficial stinging when open to air during dressing changes
venous ulcer: pulses
Usually present with only venous etiology but may be difficult to palpate with edema
what is the pathophysiology of VTE/PE
it’s unknown
VTE =
blood clot that forms in the “deep veins”
PE =
blood clot in the arteries of the lungs
Virchow’s tirad evidence
stasis of blood, vessel wall injury, and altered coagulation
platelet aggregation can lead to ___ ___
pulmonary embolism
risk factors for vte/pe
- blood pooling AFIB blood pools in top chambers of heart
- surgery - immobility; distrupting hemostasis
- cardiovascular disease
- cancer
- sickle cell disease
- trauma to vein
- recent childbirth; pain
- oral contraceptives; prolonged mechanical ventilation (PE); IV drug use; tobacco use
- hormone therapy; corticosteroids; recent bone fracture; travel/been on a plane
- Virchow’s triad
3 parts of virchow’s tirard
- venous stasis
- endothelial damage
- blood hypercoagulability
what is venous stasis
immobility; dysfunctional vein valves; changes in blood flow
what is endothelial damage
releases clotting factors
what is blood hypercoagulability
increase in fibrin production; oral contraception, chemo
what are the manifestations for VTE/PE
- unilateral leg edema
- pain
- hemoptysis
- low grade fever 100.4
- brown color with venous ulcer - stasis dermatitis
- redness/swelling/warmth
- pulmonary embolism - sudden or new onset of SOB
- hurts when breathe
- cramping in legs, tender, dull achy - typically in calf. warm to touch
what is Homan’s sign
pain in calf during dorsiflexion
labs for vte/pe
- prothrombin time (PT)/international normalized ration (INR)
- aPTT
- platelets
- h/h: hemoglobin & hematocrit
- D-dimer
what is prothrombin time and normal range
time measured for blood to clot
11-13.5 sec is normal range
this is used for herapin, this is sensitive test to make it more accurate
aPTT
waht is the normal range for aPTT
20-45 seconds
this is important for clotting. if not clotting puts pt at risk for bleeding
platelets
measuring function of capable of carrying oxygen to tissues
hemoglobin & hematocrit
do we want hemostasis in the body
yes
this can indicate a clot is there and is breaking down.
d-dimer
this can be an indication of PE, pregnancy.
less than ____ can rule out PE
d-dimer
less than 500
diagnositcs for vte/pe
duplex ultrasound
sprial ct scan - ct angio
v-q scan (ventaliation/perfusion scan)
this examines the blood flow in major arteries and veins in the arm and legs
duplex ultrasound
this is uses a dye to see blow flow. with dye you can see structures, see if th re is tissue damage
spiral ct scan - ct angio
nursing considerations for spiral ct scan
-if pt is aware of any allergies to dye
-any renal deficiencies
-pt given IV fluids
administers radioactive subustance via inhale & IV to see how much pts getting to see if theres a mismatch and where issue lies
v-q scan
if performing diagnostic test for vte/pe and pt is pregnant which test do you do
v-q scan
RN interventions for vte/pe
- prevent thrombus from start
- monitor lab values
- early and frequent ambulation
- compression socks
- cardiac enzymes
- elevate legs
- check for bleeding risk
- pain medicaton
- check cap refill
if pt has VTE what RN intervention do you NOT do
dont’ use socks or SCDs bc it will break it off and send it to the heart or lungs
elevating legs does what for vte/pe
raising legs decrease swelling and help with venous returns.
what medications do you use to treat vte/pe
heparin , warfarin, enoxaparin
what lab do you use to monitor heparin
what is the antidote
how would it be administered
PTT or aPTT
protimin sulfate
sub q or IV - two inches below umbilicus
warfarin - what is the lab used to monitor it
what is the antidote
how administered
PTINR
Vitamin K
Is pill only
enoxaparin - what lab is used to monitor med
none - look at CBC or platelets
what are the nursing interventions for heparin, warfarin, enoxaparin
- look for bleeding
- swallowing capability
- check diet to make sure they aren’t ingesting too much vitamin K
collaborative goals for vte/pe
pain relief
medication compliance
decreased edema for pts with VTE
no skin breakdown
safety considerations for VTE/PE
- bleeding
- BP - watch for low if pt is bleeding, HR will go up
- avoid IM injections
- check for delayed cap refill, confusion, mental status changes
- notify dentist/provider if having surgery/procedure
- dont stop taking meds
- decrease edema, no skin breakdown - can cause venous ulcers if have skin breakdown
- teach about prevention
- nutrition therapy
- ambulation, ROM exercise, reposition pt every 2 hours if can’t get out of bed
A 69-year-old man has been identified as having peripheral artery disease (PAD) and is motivated to slow the progression of the disease. Which of the following measures addresses the most common underlying cause of PAD?
Making lifestyle changes that address atherosclerosis
Atherosclerosis is implicated in the etiology of PAD. Hypertension and low activity levels may also exacerbate or contribute to the disease, but these are less significant than arteriosclerosis. Increased intake of antioxidants has not been shown to affect the course of PAD.
An obese patient with a history of smoking and hypertension underwent a coronary artery bypass graft for the treatment of coronary artery disease. During the patient’s postoperative recovery, he developed a DVT. The development of this event was a result of the interaction between which of the following pathophysiological phenomena? Select all that apply.
- Stasis of blood resulting from immobility and surgery
- Injury to one or more of the patient’s vessel walls
- Cardiac stress resulting from surgery
- Alterations in the normal process of coagulation
- The presence of an inflammatory process
1, 2, 5
-Stasis of blood resulting from immobility and surgery
-Injury to one or more of the patient’s vessel walls
-The presence of an inflammatory process
Which observation regarding ulcer formation on the client’s lower extremity indicates to the nurse that the ulcer is a result of venous insufficiency?
Large and superficial
Ulcerations are in the area of the medial or lateral malleolus (gaiter area) and are typically large, superficial, and highly exudative. Superficial venous insufficiency ulcers cause minimal pain. The base of a venous insufficiency ulcer shows a beefy red to yellow fibrinous color.
A woman has sought care from her primary care provider, stating, “The front of my foot aches constantly these days, and it’s gotten so bad that it keeps me up at night.” The nurse should recognize that this patient may be experiencing the symptoms of:
Severe arterial insufficiency
A client is being discharged following pelvic surgery. What would be included in the patient care instructions to prevent the development of a pulmonary embolus?
Tense and relax muscles in the lower extremities.
A client is being discharged home with a venous stasis ulcer on the right lower leg. Which topic will the nurse include in client teaching before discharge?
Application of graduated compression stockings
Graduated compression stockings usually are prescribed for clients with venous insufficiency. The required pressure gradient is determined by the amount and severity of venous disease. Graduated compression stockings are designed to apply 100% of the prescribed pressure gradient at the ankle and pressure that decreases as the stocking approaches the thigh, reducing the caliber of the superficial veins in the leg and increasing flow in the deep veins. These stockings may be knee high, thigh high, or pantyhose.
The nurse is caring for a patient with peripheral arterial insufficiency. What can the nurse suggest to help relieve leg pain during rest?
Lowering the limb so that it is dependent
Persistent pain in the forefoot (i.e., the anterior portion of the foot) when the patient is resting indicates a severe degree of arterial insufficiency and a critical state of ischemia. Known as rest pain, this discomfort is often worse at night and may interfere with sleep. This pain frequently requires that the extremity be lowered to a dependent position to improve perfusion to the distal tissues.
Which risk factor is related to venous stasis for deep vein thrombosis (DVT) and pulmonary embolism (PE)?
Obesity
Obesity is a risk factor for DVT and PE related to venous stasis. Trauma, pacing wires, and surgery are related to endothelial damage as a risk factor for DCAT and PE.
