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Intravenous access
pathway directly into the intravascular fluid space either in a peripheral vessel(PIV) or a central vessel (CVAD).
Vascular Access Device Selection
Duration: PIV for shorter, CVAD for longer
Patency: PIV more at risk of loss of patency
History of vascular access and comorbidities: difficult prior access, skin, vessels
Type of therapy: vesicant/irritants, pH
Patient’s preference
*Always select smallest gauge appropriate (typically 22 for PIV) and minimumlumens
Phlebitis
inflammation of vessel wall
warmth, pain, swelling, redness at insertion site
Infiltration + Extravasation
Infiltration: Leakage of non-vesicant (non-irritating) solutions or medications into surrounding tissue.
Extravasation: Leakage of a vesicant (irritating or tissue-damaging)
Pain, Swelling, cool to touch
vesicant = Can cause severe tissue damage, blistering, or necrosis
PIV-related thrombosis
clotting at/from insertion site
Swelling, pain, difficulty moving limb at insertion site, if thrombosis moves --> pulmonary embolism (decreased O2, SOB)
PIV – related bloodstream infection:
infection originating from device —> catheter, insertion site, IV system
Pain, swelling, fever, purlent drainage at site
usually localized infection, may progress to bloodstream infection
CVAD infection much more serious = systemic infection
VAD Selection: PIV
Access in upper extremity
Short term therapy (<7 days)*
Monitor for repeated failed/loss access = may consider switching to another VAD or site
VAD Selection CVAD
Use when suitable PIV access is unavailable
Long term therapy
Suitable for vesicant/irritant medications/nutrition
Central Venous Access Devices
Inserted into a large vein in the central circulation system, where the tip of the catheter terminates in the superior vena cava (SVC) that leads to an area just above the right atrium
Inserted by HCP with specialized knowledge
Often inserted with ultrasound guided technique
Common CVADs:
Peripherally Inserted Central Catheter (PICC)
Non tunneled CVAD
Tunneled CVAD
Implanted CVAD
PICC
Enters body on upper arm, catheter runs to superior vena cava
VERY common in clinical settings
RNs can insert and remove(specialized skill!)
Medium term use
Non-Tunneled CVAD
Enters body directly at vessel site (internal or externaljugular, subclavian, or femoralvein), catheter runs to superior vena cava
Catheter outside of the body at the insertion site
Common in critical care patients (shorter term) = emergency access areas
NOT appropriate to leave in —> pts wont be discharged with, inconvienent
HIGH risk of infection = short distance outside to circulation
Tunneled CVAD
Tunneled (Hickman, larger or Broviac, smaller)
Proximal end tunnelled subcutaneously from the insertion site and brought out through the skin at an exit site. Antimicrobial cuff (under skin, not at enterance)
Long term use
Implanted CVAD
Implanted (Port-A-Cath)
port = small disk, top is self-sealing silicone septum
catheter connected to port —> central vein
Device may be placed in the chest, abdomen, or inner aspect of the forearms
under skin, not visible (may appear as bump, palpable)
Accessed by special needle(specialized skill!) = after needle removed no dressing needed
Long-term use (longest out of all CVAD)
CVADs - Infection
Infections=high risk for sepsis!
Patient populations
peds, oncology (chemo, blood draws), ICU, immunocompromised
PPE
gloves for routine access, dressing change
mask, gown, gloves insertion, per protocol
Anti-Microbials
caps, dressings
CVADs - Infection Risks and Signs
INFECTIONS = HIGH RISK FOR SEPSIS = directly into bloodstream
Maintain sterile technique when using CVADs—remember they are a directportal to the central vasculature
What signs and symptoms of infection should you notice? Swelling,redness, purulent drainage, pain, fever
If you notice S/S of infection – notify the healthcare provider!
You might also notice signs and symptoms of phlebitis – redness, redtracking vessels from device, swelling – if you notice these, stop the infusion and notify the provider!
Using a CVAD: placement + flush
consider placement (confirmed placement?)
Flush prior to and after use with pre-filled 10mL syringe
prior to ensure patency, after to ensure meds r delivered
Do NOT push past resistance
could be clot = stroke, or pushed again vessel wall (damage)
Report resistance to provider (may order a medication that is instilled into the CVAD to try and breakdown a clot in the CVAD prior to reinsertion)
TPA or TNK
Using a CVAD: Lock
“Lock” with heparin **
When CVADs are having a period of unuse – say between treatments, the CVADs can be locked with a heparin flush that is left in the CVAD tubing to prevent clotting and occlusion
keeps positive pressure, overwise blood can back up into line and clot
Look for labels/orders before use!
heparin NOT FLUSHED!, must be aspirated out then flush w saline
CVAD - Air emboli
Findings: Sudden onset chest pain, SOB, dizziness
LARGE bolus of air, can obstruct circulation
Action: IMMEDIATE: L lateral Trendelenburg (trap air in R atrium, to prevent movement to brain, heart, lungs, etc), and administer O2
head down, left side
air bubble made of nitrogen, O2 causes conc gradient, nitrogen from bubble into blood (smaller bubble)
aspirate air out if needed (large)
The nurse is providing health teaching to the parents of a child withleukemia about their central venous catheter device and it’sassociated care. Which of the following statements made by theparents indicate a need for further health teaching?
A“We will cover the site with a transparent adherent dressing.”
B“We will report if there is swelling or drainage at the exit site.”
C“We will use clean technique when changing the dressing.”
D“The nurse will flush the device before and after administration.”
C = sterile technique
A nurse is assessing a client with a central venous access device(CVAD). Which of the following findings should the nurse identify aspossible signs of a CVAD-related infection?
Select all that apply.
A. Redness and warmth at the insertion site
B. Fever and chills
C. Increased capillary refill in the extremities
D. Purulent drainage from the catheter site
E. Sudden onset of hypotension
F. Bradycardia and cool skin
A, B, D, E
Will be decreased cap refill
Signs of septic shock --> INCREASE HR, RR, progressing to LOW BP
Bradycardia + cool skin --> end stage sepsis
Sodium (135-145 mmol/L):
closely linked to fluid balance (BP, volume), nerve/muscle func
correct slowly to prevent cerebral edema
Sodium replacement must be slow --> water follows sodium --> can leave to fluid overload (cerebral edema)
mild imbalances are corrected with isotonic solutions = replaces both sodium + fluid w/o shifting fluids in/out cell
signficant imbalances can be corrected with hypo/hypertonic sodium containing fluids
Potassium (3.5-5 mmol/L):
potassium maintains resting electrical charge for cardiac cells (too high = less excitable, too low = hyperexcitable), muscle elec activity (contract), pH
high alert
concern for cardiac instability
mild imbalances may be corrected with oral replacement or excreting medications (diuretics)
significant imbalances may be corrected slowly (not IV push!) with IV potassium
connect to cardiac monitor
What do we want to know about electrolyte imbalances?
There is LOTS of overlapping symptoms
Focus on what is unique and different from 1 electrolyte toanother
Focus on what is opposite between hypo and hyper
Chloride 95-105 mEq/L
Involved in blood pressure and blood volume maintenance and pH balance
Na+ and Cl- are friends and they move around together (also water)
Cl- and HCO3- are NOT friends —> opponents
since they are both anions, if one is low other will move to compensate (electrical neutrality)
HCO3- = Basic substance that ↑pH
Cl- moves from plasma into cells and HCO3- moves into plasma
This shifting can be another buffer system to manage pH changes
alkolosis = vomiting (HCl lost = bicarb left behind), diuretics (excrete Na, K, Cl)
acidosis = diarrhea —> bicarb in intestinal secretions
H+ and K+ relationship
inverse relationship (both pos)
Acidosis (↑H⁺ in blood): H⁺ enters cells (to try buffer pH) → K⁺ leaves → hyperkalemia
Alkalosis (↓H⁺ in blood): H⁺ leaves cells → K⁺ enters → hypokalemia
Magnesium 1.3-2.1 mEq/L
Abundant Intracellular Cation (just like K+)
Involved in neuromuscular contractility (with Ca+, 2:1, more mag) = mag is for muscle RELAXATION, calcium = contraction
works w calcium for myocardial func + vascular tone
Neuromusclar junction (NMJ) --> ACh crosses synaptic cleft —> binds to receptor —> contraction, magnesium blocks ACh release (no muscle conc)
Hypermagnesemia
Hypermagnesemia
Signs/Symptoms: Common Symptom:bradycardia, ↓ BP, weakness, ↓DTRs (deep tendon reflexes), lethargy —> coma
Causes: Increased Intake – antacids or laxatives (mag stays in gut to draw water = diarrhea), too much IV, Decreased Excretion – renal disease
Treatment:
Diuretics
Hypomagnesemia
Signs/Symptoms: tachycardia & HTN,twitching, paraesthesia (tingling, numbness), hyperreflexia (positive Trousseaus’s & Chovstek’s signs), Irritability & confusion
Causes: Insufficient Intake –malnutrition,Celiac, Crohn’s, vomiting, diarrhea; Excess Excretion – diuretics, alcohol use disorder
Treatment:
mag replacement
Magnesium Replacement
Oral Replacement (Asymptomatic)
MgOxide or MgSulfate (may cause diarrhea)
IV Replacement
Use MgSulfate —> slowly (arrhythmias)
Monitor for ↓Deep Tendon Reflexes
NOTE: Calcium and magnesium are also often friends —> If you have too little magnesium, you may also need to restore Calcium
Calcium 9.0-10.5 mg/dL (4.5-5.3 mEq/L)
Important role in muscle contraction, stabilizing cell membranes (neuromuscular excitability)
Absorption depends on Vit D
Friends with Magnesium, same reflected values (ex. calcium up, mag up)
Calcium stables resting membrane potential --> too much wont be able to control depolarization (not going to open as much), less active potentials
INSIDE cell —> contracts
OUTSIDE cell —> less action potentials (too much)
Hypercalcemia
High extracellular (blood) Ca²⁺ stabilizes voltage-gated sodium channels → fewer action potentials → muscles fire less → weakness
Signs/Symptoms: decreased reflexes,N/V, bone pain/fractures,confusion/lethargy, weakness
Causes: hyperparathyroidism, cancer,prolonged immobilization, Vit D overdose, acidosis, excess dietary intake
Treatment:
Urinary excretion
Increase weight baring topromote bone mineralization
Hypocalcemia
Low extracellular Ca²⁺ → sodium channels less stabilized → more spontaneous action potential
Signs/Symptoms: paresthesia around mouth, hyperreflexia, muscle cramps, Chvostek’s (facial twitch when tapping) and Trousseau’s sign (carpal spasm when inflating BP cuff for ~3 mins) ,seizures, confusion/lethargy
Causes: thyroidectomy, vit D deficiency, kidney disease, alkalosis,alcoholism, laxative misuse,inadequate dietary intake
Treatment:
Oral (Dietary supplement), or
IV if severe
Phosphate 3-4.5 mg/dL
Important role in nerve and muscle function, RBC production, bones+teeth
ATP production relies on phosphate
in bone calcium + phosphate bind together —> calcium phosphate
Inverse relationship with Calcium
if both r high in blood —> can form crystals in soft tissues
PTH raises blood calcium (from bone), kidneys excrete phosphate
Hyperphosphatemia
Signs/Symptoms: hypocalcemia,depression/anxiety, muscle cramps
Causes: kidney disease, chemo,laxative use, hypoparathyroidism,excess dietary intake
Treatment:
Treat underlying cause
Treat hypocalcemia
Administer phosphate binding agents (get excreted in stool)
A nurse is caring for a client who has chronic kidney failure andhypoparathyroidism. The client has been admitted for 5 days, andrecently stated to the nurse “I feel tingling around my mouth, and mylegs are aching!” Which electrolyte imbalance would the nursesuspect?
A. Hypokalemia
B. Hypocalcemia
C.Hypernatremia
D. Hypercalcemia
B.
The nurse is reviewing the intake chart for a new admission andnotes their most recent magnesium level is 3.6 (reference range=1.3-2.1 mEq/L). The nurse notes this patient’s assessment findings thatmay be may be associated with this result? Select all that apply.
A. BP 106/64 mmHg
B. Muscle twitching
C. Lethargy
D. HR 44 bpm
E. Hyperreflexia
A C D
What is enteral nutrition? + indications
Provides liquified foods into the GI tract via a tube
Indications:
When the GI tract is functional, but oral intake is not meeting nutritional requirements
May be required for pts with swallowing disorders, burns, trauma,organ failure, severe malnutrition
Gastrointestinal Intubation
Uses
Deliver enteral nutrition, or
Remove gastric contents with suction
Different Types of Tubes
OG, NG & G-Tube (PEG) —> end in your stomach
SBFT & J-Tube —> aka post pyloric feeding tubes —> end somewhere in your intestine
Orogastric Tube (OG)
Inserted orally and tip is in the stomach
Large diameter
ER or ICU (unconscious clients)
Suction
end in stomach
Nasogastric Tube (NG)
Inserted nasally and tip is in the stomach
Moderate diameter (suction) to small diameter (feed)
Suction + Enteral Feeding
Short Term < 4 – 6 weeks
in stomach
Gastrostomy Tube (G-Tube)
Surgically inserted - tube passes through the abdominal wall into the stomach
Large diameter
Feeding
Long-Term
ends in stomach
Small Bowel Feeding Tube (SBFT) / nasoduodenal tube
Inserted through nose and tip is in the duodenum
Small diameter
Feeding
Medium Term < 4 – 6 weeks
ends in intestines
bypass stomach, reduce risk of aspiration
NEVER ASPIRATE + NEVER check residuals (doesn’t store food/fluid like stomach, intestinal wall more delicate)
feeding tolerance checked —> abdo distention, cramping, N/V
Jejunostomy Tube (J-Tube)
surgical procedure —> tube passes through the abdominal wall into the jejunum of the small intestine
Larger diameter
feeding
Long-Term
NEVER ASPIRATE + CHECK RESIDUALS
bypass stomach = reduce risk of aspiration
GI Intubation Insertion: General Steps
Assess Safety – are there contraindications?
Review Order
Collect Supplies
Prepare the Patient and the Environment
Insert per agency protocol
Check placement before use– method to verify placement is dependent on agency. Likely to involve x-ray, other methods include aspirating for gastric contents and measuring pH, or may involve air instillment and auscultation
Air instillment and auscultation + aspirating are often prone to failure --> xray important
you may not be the one inserting it but before using it, make sure where it is supposed to be
Enteral Feeding types
Multiple types of enteral feeding methods, dependent on client, needs, setting
All as prescribed by provider, dietician
Bolus: resembles normal meal patterns, formula is administered of 30-60 minute period every 3-6 hours
Continuous: Feeding administered continuously over 24hours via infusion pump
Cyclical: feeding is administered in daytime or night time hours over 8-16 hour period
Enteral Feeding Steps
Confirmation order? Site? Length?
Assess bowel sounds prior to feeds
Flush prior to feeds for patency (typically 25-40mL)
Position the client appropriately to prevent aspiration—semi/high fowler’s/reverse trendelenberg. Min 30-45 degree
during feed + 30 mins after
Aspirate residual volume and return contents to stomach PER ORDER
to ensure things move appropriately + pt tolerating well —> lots of volume = gastric paresis (could be)
Warm feeds to room temp to prevent diarrhea or cramps
Change tubing every 24 hours
Hang 4 hours of feed at a time to prevent bacterial growth
Flush after feeds
Administer other flush per agency policy/pt orders
free water flushes
Extra amounts of sterile or tap water (as ordered) given through a feeding tube in addition to formula.
Maintain hydration — some formulas don’t provide enough free water.
Prevent clogging of the feeding tube.
Help meet fluid requirements, especially when feedings are concentrated or cyclical.
Enteral Feeding Considerations
Provide appropriate and routine oral care!
Often overlooked when patient is not taking intake by mouth
Need to clean, moisten, maintain oral health
When initiating first enteral feeds, ensure routine monitoring of fluid balance (daily weights, I/O q hourly with first admins *think what would happen if it went many hours without checking and something was wrong!) until reached stability
pt could b confused = pull out tube
aspirate, unable to tolerate
Changes to respiratory status when administering enteral feeds may = aspiration – STOP feed and assess!
difficulty breathing, gurgling sounds, abnormal lung sounds
Enteral Medication Admin
Use liquid medications where possible
Crush tabs thoroughly
Empty capsules (CANNOT b crushed)
Do not administer any coated medications (DONT CRUSH!)
e.g. enteric coated --> meant to break down in small intestine not stomach
Dissolve meds in water
Flush prior to and after medication administration
Consideration – you do not want to fluid overload the client.Ensure you are accurately calculating all the flushes you are giving. If you give medication flushes, subtract from routine flushes
Gastrointestinal Suctioning
Decompress stomach by removing fluids or gas to promote abdominal comfort
Bowel obstruction --> stomach is still making gastric juices + gas (can be uncomfortable) --> suction out
Decrease risk of aspiration
Suction settings between 0-80 mmHg, typical 40-60 mmHg
Suction Types
Continuous/Straight (Immediate removal of contents)
emergency (can be dangerous)
risk of injury to mucosa
Low-Intermittent (Prolonged decompression)
starts and stops
Gastro Tubes: Nursing Assessments NG & SBFT (sunction)
Location —> Has it moved? What number is it at? Does itneed reinforcement?
Patency —> Is it draining? – if not; flush to clear blockage.
may be on the mucosa = reposition patient
Drainage —> volume, colour? --> 125 mL/hr would be !!!
125 ml/hr = can impact intravascular fluid
+/- Feeds, Flushes & Residuals (if they r ordered)
Mucosa and skin Integrity?
Gastro Tubes: Nursing Assessments G-Tube & J-Tube (sunction)
Patency
Feeds, Flushes & Residuals (check for)
Skin Integrity? Daily site dressing change? – goal: keep stoma dry!
Aspiration Pneumonia
Fluid + food into alveoli not allowing gas exchange, carries bacteria
Fever and increasing WBC
SOB, increased RR, SpO2
Confusion
Abnormal breath sounds —> diminished or crackles
can lead to sepsis
Prevention: Keep HOB elevated> 30 for feeds and following
GI Related
Nausea, Diarrhea, Gas
Change feed type? More fiber?
Dietitian --> to change feed
Constipation
Bowel protocol Initiation? —> laxatives, fluids, stool softener etc. (per provider order)
Dumping Syndrome
food rapidly goes into small intestine without digestion (in stomach)
Fullness/Distention, N&D
FVD (dry vascularly) —> tachycardic, hypotensive
Lot of hypertonic solution/food entering + undigested glucose
causes fluid to enter intestine —> takes away from fluid volume (veins)
flucuations in glucose
Blocked Tube
Follow protocol
Blocked tubes may be flushed with pancreatic enzymes dissolved in sodium bicarbonate
Need to consult provider for order
breaks down congealed feed
DO NOT PUSH if there is resistance (mucosa injury) —> flushing + repositioning insstead
If tube blockage cannot be relieved —> change NG or SBFT to prevent nutrition disruption
try not to change surgical tubes
Removal: Nursing Considerations
Short – medium term --> e.g. nasal tubes (surgical usually not removed)
Consider clamping for a trial before removal
In case N, V and distention return
Flush with sterile water then remove
Never force or tug
stomach contents still in tube can go into mouth/sinuses (if not flush)
Support the client in oral care
Parenteral Nutrition (PN)
Administration of nutrients via the bloodstream when the GI tract is unusable
Indications: Non-functional GI tract, malabsorptionsyndrome, severe burns/trauma
Tailored to patient needs; composition changes withpatient condition
Components:
Base Solutions: Dextrose and amino acids(protein)
Additives: Electrolytes, vitamins, trace elements
Methods of PN: Central Parenteral Nutrition (CPN):
AKA total PN
Long-term support or high protein/energy needs
Administered via central venous catheter or PICC
Requires large central vein for rapid dilution
very hypertonic solutions = rapid dil prevents vein irritation
Methods of PN: Peripheral Parenteral Nutrition (PPN):
Short-term support, lower protein/energy needs
Administered via peripheral catheter or vascular access device
Less hypertonic, risk of phlebitis (smaller veins) and fluid overload (PPN solutions need to be dilute = more fluid volume given)
Complications of Parenteral Nutrition
Catheter-related issues
Refeeding syndrome: occurs in patients during initial nutrient re-introduction following significant malnutrition = body taking nutrients from fat + muscle not used to glucose = insulin secretion starts
Characterized by electrolyte shifts (into cell) –predominantly: LOW phosphate, LOW potassium —> in blood
Fluid imbalances = fluid goes into cells = low blood volume, BP
Blood glucose instability – close monitoring
Nursing Considerations: Parenteral Nutrition
Nursing considerations:
Closely monitor fluid balance until stable – daily weights, intake and output monitoring, assessment for S/S of hypo/hypervolemia
Wean on and off – gradual rate increases
Routine CBC and electrolyte monitoring – q 2 days until stable with changes to PN composition in response
Clients must tolerate 60% of caloric intake via GI tract to warrant discontinuation without =malnutrition
ensure stability + meeting caloric needs
The nurse is developing a care plan for a client with a g-tube (PEG)tube. Which of the following are appropriate interventions for thenurse to include? Select all that apply.
A. Use a dry, sterile dressing at the PEG tube site
B. Add a maximum of 12 hours of feeding product at a time toprevent bacterial overgrowth
C. Maintain semi-fowler’s position for feedings
D. Monitor weight, and intake and output
E. Flush tube every 72 hours
A, C, D
B. = q 4 hrs
D = should be flushed before and after feds, taking meds etc.
A client with acute pancreatitis has a nasogastric tube in place for gastric decompression. The nurse notes that the client’s abdominal distention has increased and there is minimal output from the nasogastric tube. What is the most appropriate action for the nurseto take next?
A. Increase the suction pressure
B. Flush the NG tube
C. Notify the provider
D. Disconnect the suction
B. Blockage of tube --> flush
Don’t disconnect without provider order