EXAM 3 Flashcards
Gas exchange relies
adequate perfusion of alveoli
ventilation vs perfusion
Ventilation = air coming in
Perfusion = blood flow to the capillaries
“alveolar dead space”
shunt unit
silent unit
a. “alveolar dead space” = alveolar not perfused -> no gas exchange occurring
Examples: PE and pulmonary infarct
b. “shunt unit” = alveoli not ventilated but perfusion intact -> perfusion > ventilation
Examples: pneumonia and atelectasis
c. “silent unit” = perfusion AND ventilation impaired
Examples: ARDS and pneumothorax
how is O2 transported
Oxygen transported in 2 ways:
1. 97% bound to Hgb (aka O2 saturation)
2. 3% dissolved in serum
what does a shift in the oxyhgb curve mean
that affinity of Hgb to O2 is changed
shift to the left
3 meanings and the factors
Hgb HOLDS onto O2
Increased O2 saturation
Impaired O2 delivery to tissues
Factors that shift the curve to the Left:
Low temperature (hypothermia)
ALkalosis (a rise in pH)
Low CO2
Low 2,3 diphosphoglycerate (in septic shock, hypophosphatemia, and blood transfusions)
shift to the right
3 meanings and the factors
Hgb has LESS affinity for O2
Decrease in O2 saturation
Brief temp increase in O2 delivery to tissue
HgB RELEASES O2 MORE READILY
Factors that shift the curve to the Right =
Rise in body temperature (fever)
Reduced pH (acidosis)
Rise in CO2 (hypercapnia)
Rise in 2,3 diphosphoglycerate
ph
measures hydrogen concentration in blood. Normal 7.35-7.45
SaO2
percent of hemoglobin saturated by O2. Normal 93-97%
PaO2
pressure of O2 in the blood. Normal 80-100 mmHg
PaCO2
tension of dissolved CO2 gas in arterial blood. Regulated by the lungs (respiratory process). Thought of as acid in interpreting ABGs. Normal 35-45 mmHg
HCO3
bicarbonate, main base in serum, helps regulate pH because it can accept hydrogen. Regulated by kidneys (metabolic process). Normal 22-26 mEq/ml
what is ARDS
SUDDEN, ACUTE, PROGRESSIVE form of acute respiratory failure = alveolar damage = HYPOXIA
3 steps in ARDS
Injury to lungs -> inflammatory response -> alveolar capillary membrane damage
1 cause of ARDS
1 : Sepsis leading cause bc its in inflammatory process
5 things happening in stage 1 ARDS and name of stage
- Capillary membranes leak
- Protein-rich fluid fills alveoli
- Gas exchange is disrupted
- Type 1 alveolar cells are destroyed(type 1s are responsible for gas xchange)
- Hyaline membranes are formed
6 s/s of stage 1 ARDS
Normal chest x-ray, or with dependent infiltrates
Tachypnea and dyspnea
Use of accessory muscles
Lung sounds may be clear
PAWP may be < 18 mm Hg
Change in level of consciousness
7 things happening in stage 2 ARDS and name of stage
- Type 2 alveolar cells are damaged(type 2s produce surfactant)
- Surfactant production declines
- Peak inspiratory pressure increases
- Compliance declines(think lungs ability to open and relax easily and smoothly)
- Decreased FRC (functional reserve capacity – ability to take an extra deep breath when needed)
- Further loss of alveolar function
- Ventilation/perfusion mismatch
7 s/s of stage 2 ARDS
fibroproliferative
Chest x-ray with bilateral infiltrates and elevated diaphragm
Refractory hypoxemia and hypercarbia despite hyperventilation
Dramatically increased WOB
Crackles on auscultation(crackles means fluid in alveoli – diuretics wont always work which usually does in other conditions )
Rhonci on auscultation means fluid outside of alveoli which coughing and deep breathing can help – or if mechanically vent. – need to be suctioned
PAWP, RA (CVP) increase
Right-sided heart failure develops - peripheral edema
Agitation
4 things happening in stage 3 ARDS and name
Development of fibrotic tissue in the ACM resulting in alveolar disfigurement
- Decreased lung compliance
- Worsening pulmonary hypertension
- Increased dead space ventilation
8 s/s of stage 3 ARDS
Leukocytosis and fever
Elevated WBC
Worsening infiltrates on chest x-ray
Worsening hypoxemia and hypercarbia
Decreased tissue perfusion
Increasing HR with decreasing BP
Lactic acidosis
End-organ dysfunction
goal of mechanical ventilation
The goal is to use the least amount of O2 needed (ideally < 60%) to keep SaO2 88-95%, and P/F ratio>200
are abx used for mechanical vent
only if infection
10 treatments of ARDS
mechanical vent
prone position, up in chair
ionotrpic meds for hemodynamic monitoring
mild fluid restriction, NG tube, PPIs
relieve bronchospasm albuterol
reduce air inflammtion salumetrol IV steroid
reduce pulmonary congestion
reduce anxiety
PEEP
check Hgb
4 reasons mechanical vent is used
IMV/ACV for respiratory rate
FIO2 to meet needs while aim is < 60%
restricting tidal volume to 4-8 mL/kg
pressure ventilation/PEEP to enhance gas exchange
ACV
patient receives a set tidal volume and breaths if patient’s own effort falls below set rate
SIMV
patient receives a set number of breaths with a set tidal volume, but with any additional breaths the patient’s effort determines tidal volume and allows use of respiratory muscles.
PEEP
at the end of expiration, it will deliver pressure to keep lungs open for longer to facilitate gas xchange instead of always adding O2
rapid sequence of intubation meds
- anesthetizing agents with a short half-life (diprivan (Propofol), midazolam (Versed), or etomidate
- paralytics such as succinylcholine, rocuronium
- long-term anesthetics and analgesics to reduce anxiety and promote comfort of the patient while intubated
diprivan - class, use, monitoring
- very short-acting anesthetic
- no analgesic properties
- less amnesia properties than benzodiazepines
- continuous infusion, titrated slowly
- Monitor for hypotension and lipid levels (after 2 days of infusion)
- High or excessive doses may result in Propofol infusion syndrome, hypotension, and zinc deficiencies.
10 nursing actions for intubation and ventilation
- Explain procedure
- Monitor oxygenation and cardiovascular status - alert hcp if o2 <90
- Administer medications
- Auscultate lungs to check for air movement after tube placement
- Utilize CO2 detector to verify placement
- Secure tube
- Note placement mark on the tube for future monitoring
- Monitor for patient awakening as the chocking sensation associated with the tube will create anxiety
- Chest x-ray following intubation is required to verify correct placement
- We want end of tube 0.5 cm above corina (C in pic) to ensure getting air to both side
how to prevent barotrauma in mechanical vent 2
- Use of lower tidal volumes (remember this is amt of air coming in from ventilator) (4-8 mL/kg of body weight) and permissive hypercapnia – prevents barotrauma and volutrauma
- Use of inverse ratio ventilation (IVR) – promotes slower delivery of tidal volume and helps prevent barotrauma
1 prevention of VAP
hand hygiene
9 ways to prevent VAP
- Hand hygiene #1
- Elevation of the head of the bed > 30 degrees to prevent aspiration
- Daily sedation vacations and assessment of readiness to extubate
- Peptic ulcer disease prophylaxis – histamine blocker( -tidines) or PPI (omeprazole)
- Deep vein thrombosis prophylaxis
- Oral care with chlorhexidine
- Suctioning using in-line system to prevent infection – remember suctioning used when you hear rhonci or if you see secretions in the tubing coming up
- Continuous subglottic suctioning
- No routine change of ventilator circuit
5 safety protocol for mechanical ventilation
- Suctioning to clear secretions as indicated, assessing need every 2-4 hours
- Response to ventilator alarms
- Appropriate use of restraints
- Facilitating communication – VS, body language, white boards, hand gestures
- Providing education
8 readiness to wean and extubate
- Adequate muscle strength and endurance- breathe long enough and strong enough on
- their own, can they cough up secretions? How much secretions?
- Clear lungs
- Stable cardiac/hemodynamic status
- Adequate nutritional status – adequate protein and calories
- Adequate hemoglobin
- Stable neurological status
- Spontaneous weaning trial – patient is placed on a T-piece, removed from the ventilator and connected to a humidified oxygen source and indicators are monitored
2 types of pneumothorax
- Closed – rupture of blebs on the visceral pleural space
- Tension – rapid accumulation of air in the pleural space resulting in extremely high intrapleural pressure with resulting tension on the heart and great vessels. A tension pneumothorax is an emergency situation.
small vs large s/s pneumot
- Small – tachycardia, dyspnea
- Large – respiratory distress, shallow, rapid respirations, dyspnea, air hunger, O2 desaturation, no breath sounds over affected area, presence of air or fluid on chest x-ray
treatment for pneumothorax
Chest tube insertion – removes air/fluid from pleural space and restores normal intrapleural pressure (negative) so lung can re-expand. Tube is inserted and connected to a drainage system
3 compartments of drainage system in chest tube
- First compartment – collection chamber
- Second compartment – H2O seal chamber
- Third compartment – suction control chamber
5 nursing actions for chest tubes
5 things to assess for sedation
a. level of consciousness, using Glasgow Coma Scale or Reaction Level Scale
b. For agitation and restlessness, using the Ramsey Sedation or Riker Sedation/Agitation Scale (RASS)
c. For anxiety
d. For sleep
e. For patient-ventilator synchrony (an indicator of comfort level)!!!!
3 classes of sedation meds with examples
a. Ativan (Lorazepam) – benzodiazepine***
b. Diprivan (Propofol) – short-acting general anesthetic***
c. Dexmedetomidine (Precedex) – an a2 agonist
ALL COMBINED WITH ANALGESIC
lorazepam - class, use, onset, SE
- benzodiazepine with anti-anxiety, sedative, and anti-convulsant effects.
- Slower onset (15-30 minutes), but longer duration (8 hours) than midazolam.
- Side effects include reversible renal tubular necrosis, lactic acidosis, hyperosmolar states, and delirium.
- Physical and psychological dependence can develop.
- Is not a first-line choice due to the risk for delirium.
dexmedatomidine - class, use, SE and tx of SE
- for short-term sedation, having anxiolytic, anesthetic, hypnotic
amd analgesic properties - Recommended for use of less than 24 hours.
- The most common side effect is hypotension requiring fluid replacement and slower administration
- Symptomatic bradycardia and heart block may develop, but usually resolve spontaneously.
how and when to assess for delirium
Assessment using the Confusion Assessment Method of the Intensive Care Unit (CAM-ICU) should be done at least once/shift.
6 nonpharm interventions for delirium and what is priority
A – analgesia: assess, prevent, manage pain / assess readiness to extubate
B – both SATs and SBTs: stop drugs, stop ventilator
C – choice of analgesia and sedation, cognitive stimulation (music), catheter removal
D – delirium: assess, prevent, manage
E – early mobility** and exercise, ROM exercise, low stimulation environment
F – family engagement and empowerment, facilitate sleep
what occurs in sepsis
infectious organism as WBCs release proinflammatory cytokines
The endothelium is affected and the coagulation system and complement systems are activated.
thrombin is produced, which causes additional inflammation
new endothelial damage along with a pro-coagulant state.
Fibrinolysis is delayed
Capillary and endothelial damage cause profound dilation.
what is sepsis
Complex process of inflammation, thrombosis, and fibrinolysis = SYSTEMIC INFLAMMATION
6 risk factors for sepsis
> 85
immunocomp
chronic illness
invasive procedures
malnutrition
abx use
1 sepsis area for <65 and >65
> 65 urinary
<65 lungs
what is sepsis diagnostic criteria
SIRS + infection + 2 of the following:
– Chills
– Hypotension
– Decreased skin perfusion, capillary refill or mottling
– Decreased urine output
– Significant edema or positive fluid balance
– Hyperglycemia (glucose > 120)
4 assessments of SIRS
- Temperature > 38 degrees C (100.4 F), or < 36 degrees C (96.8 F) –
o WBCs > 12,000/mm3 or < 4,000/mm3
this is because people who are immunocompromised, may not have a fever or elevated WBC - Pulse > 90 bpm
- Respiratory rate > 20/min, or PaCO2 < 32
criteria for severe sepsis
dysfunction of 2 or more body systems in response to hypoperfusion
sepsis labs
- Complete Blood Count (CBC) – WBC > 12, 000/mm3, platelet count < 100,000
- Arterial Blood Gasses (ABG) – acidosis and low PaO2
- Comprehensive Metabolic Panel (CMP) – glucose > 140 mg/dL because cortisol production
- Coagulation Studies – INR > 1.5, aPTT > 60
- Liver Function Test (LFT) – bilirubin > 4 mg/dL
- Serum Lactate – > 2 mmol/L
- C Reactive Protein – > 2 standard deviations above normal
- Cultures – blood final result after 48 hours – in the meantime, use empirical therapy
- Procalcitonin – marker in blood for infection in ICU patients
- > 2 = probable sepsis
- > 10 = septic shock
how to assess SEPSIS
using SOFA (sequential organ failure assessment)
Respiratory function by PaO2/FIO2,
Cardiovascular function by MAP or use of vasopressors,
Coagulation evaluated by platelet count,
Renal function by urine output and creatinine,
CNS function by GCS,
Liver function by bilirubin (liver produces coagulation factors which in sepsis is not happening)
when should severe sepsis bundle be used time frame
3-6 hours
severe sepsis treatment bundle
measure serum lactate:
if >4 give crystalloid over 30 min
if hypotensive:
fluids then vasopressors (neph, vasopressin) for hypotension not responsive to fluids to keep MAP >80!
antibiotics after blood cultures
what is septic shock
presence of sepsis AND hypotension
3 criteria of septic shock
- Systolic BP < 90
- MAP <65
- Decrease of 40 systolic without fluid treatment response
8 treatment for sepsis
– Ventilation and O2 – avoid high tidal volumes and keep inspiratory plateau pressure < 30 cm H2O
– Fluid Resuscitation – cannot be determined based on I & O alone
– Vasopressors – norepinephrine, vasopressin
– Medications – inotropic, steroid, antibiotic
– Nutrition
– Glucose Control - > 80, < 180 mg/dL - > check every hour on insulin infusion
– Fever – when to treat? 103 or higher
– Use of a cooling blanket – keep hands and feet off of blanket
what is DIC
- NOT A DISEASE
- It is abnormal response of the clotting cascade causing profuse bleeding with depletion of clotting factors and platelets
1 cause of DIC
sepsis
2 types of s/s for DIC
– Thrombotic manifestations – cyanosis, ischemic tissue necrosis, PE, ARDS, oliguria, kidney failure, abdominal pain, paralytic ileus, CVA
– Bleeding manifestations – hematoma, petechiae, purpura, oozing, GI bleeding, hemoptysis, hematuria, bone and joint pain, headache, change in mental status
6 labs for DIC
- Platelet count – value < 50, 000
– FDPs > 40 mcg/mL, or rising values (normal < 10)
– D-dimer – values > 250 ng/mL (normal < 250), not a specific or sensitive test for DIC
– Fibrinogen – values < 100 mg/dL (normal 200-400)
– PT – any elevation is suggestive of DIC
– aPTT - > 40 seconds is suggestive, values > 70 are critical
7 treatment for DIC
– First and foremost treat the underlying cause
– Supportive measures: IV fluid replacement with necessary replacement of blood products (PRBCs, FFP, platelets, cryoprecipitate)
– Monitor function of organ systems (especially neurological and renal function)
– Monitor lab values and vital signs
– Use of heparin is controversial
– Avoid invasive procedures (including rectal temperatures) - IV sticks,
– Gentle care and protect from further injury
– Assess pain, a new pain location may indicate a new clot
what is AKI
abrupt increase in creatinine resulting from injury that causes structure or function change
5 functions of the kidney
Fluid volume status
Acid-base balance
Electrolyte concentrations
Clearance of nitrogenous and other wastes
produce erythropoietin
5 functions of erythropoetin
- stimulates the production of RBCs
- secretes renin
- regulate BP
- produce active vitamin D
- regulation of calcium balance.
what is GFR and what is normal
: rate at which filtrate is formed called creatinine clearance rate– normal is 85-135
factors that decrease GFR - 5
diabetes, CAD, HTN, CKD, shock (anything that decreases CO)
1 risk of AKI
preexisting chronic kidney disease
cause of prerenal AKI
glomeruli and nephrons in prerenal
4 assessments
due to decreased renal blood flow because of reduction in CO due to severe hypotension, hypovolemia, vasoconstriction (60% of cases)
**Glomeruli and nephrons are NORMAL
a. hypovolemia – hypotension or orthostatic hypotension, tachycardia, dry mucous membranes, poor skin turgor, flat jugular veins, weight loss, low CVP/RAP and PAWP.
b. vasodilation/CV disease – edema, ascites, weight gain, increased CVP/RAP and PAWP.
c. BUN, creatinine (and ratio), creatinine clearance, urine electrolytes, GFR decreased, and renal ultrasound.
d. Na retention
5 u/a findings of prrenal
- <400mL per day
- Concentrated urine with high osmolality
- Decreased Na < 20
- FEna <1%
- Few casts, little sediment
4 treatments for pre-renal
a. For hypovolemia – administer fluid bolus with isotonic fluid – goal is to increase urine within 10-20 min
Monitor: fluid volume overload - > dyspnea, crackles, rapid respirations, shallow respirations, JVD, tachycardia, elevated BP /CVP/PAWP
b. Restore renal function ->
Increase BP and MAP using Neph
Ionotropic meds
c. Nephrology consult
d. Avoid renal injury ->avoid nephrotoxic meds like vancomycin and gentamycin, monitor peak (30 min after admin) and troughs (1hr before)
cause of intrinsic aki
prolonged hypoperfusion of the kidney (aka prerenal failure is the leading cause) due to disturbances within the glomerulus or renal tubule (30-40% of AKI cases, with the most common etiology being hypoperfusion/ischemia)
Also: rhabdomylosis, endotoxins (breakdown of muscle fibers resulting in myoglobin release and elevated CK which then block structures of the kidney)
what happens in intrinsic aki
Oxygen delivery does not meet demand and prolonged hypoxia triggers dysfunction, inflammation, and possibly necrosis of the basement membranes and renal tubules.
5 u/a findings in intrinsic
- <350
- > Na (>40)
- Fena >1%
- Granular casts and sediment
- Dark red or cola colored urine due to the increased myoglobin
4 phases of intrinsic aki
1 – onset phase, immediately following renal injury and lasting 2-4 days. Urine output decreases to 20% of normal, BUN/creatinine increase slightly.
2 – oliguric phase, lasts 10-14 days. (Most patients will manifest oliguria, although some will not – this is termed non-oliguric AKI with > 400 mL/day). There is < 400 mL/day of urine, fluid is retained, electrolyte and acid-base balance is not able to be maintained, and nitrogenous waste is not sufficiently excreted.
3 – diuretic phase, as patients regain renal function. Urine output increases, often up to 5 L/day, with improving BUN/creatinine, acid-base and electrolyte balance.
4 – recovery phase, lasting 6 months to 1 year. Most patients return to normal function, although care should be taken to avoid renal toxins. – avoid anything that can damage kidneys in this patient
9 s/s of intrinsic aki
FLUID VOLUME EXCESS =
Rapid pulse with a bounding quality
Skin that is pale and cool
Increased BP, possibly a decreased pulse pressure
JVD and/or hepatojugular reflex
Nonpitting edema in dependent areas
Increased CVP, PAWP
Increased RR, shallow respirations, dyspnea on exertion or when supine
Crackles in the bases of the lungs
The nurse should also weigh the patient at the same time every day and maintain I&O (often assessing every 1-2 hours)
LOW Na - > seen with a change in LOC
cause of post renal aki
obstruction in urinary system – BPH, stones, tumors
s.s of postrenal aki
sudden onset of anuria <50mL/ day
1 intervention for postrenal aki
bladder scan and catheter
how to tx fluid vol excess in AKI
renal replacement therapy
how to treat hyponatremia in aki
Asymptomatic: fluid restriction
Symptomatic: diuretic with hypertonic saline for Na <110 - > monitor urine output and electrolyte levels hourly
how to treat low ionized Na in aki
(normal is 4.64-5.28)
Symptoms – mild, the patient may have numbness/tingling of the digits or around the mouth, with progression, a positive Chvostek’s (cheek one) and Trousseau’s sign and in when < 0.8, tetany (unmoving muscles) and convulsions.
a. Oral supplementation may be used for mild hypocalcemia and IV replacement for more serious hypocalcemia.
b. IV infusion of either calcium chloride or calcium gluconate with the nurse monitoring the patient’s ECG, response, and lab values.
5 ways to treat hyperkalemia
a. Administration of IV calcium (in patients not receiving digitalis) may be helpful to temporarily counteract the effects of high K allowing time for other measures.
b. IV dextrose (50g), insulin (5-10 units), and NaHCO3 (50-100 mEq), often given together one after another to temporarily shift K into cells, allowing time for other measures. Inhaled beta agonists used less frequently (like albuterol) is an additional option.
c. Cation exchange resin, sodium polystyrene sulfonate (Kayexalate) to decrease total K through GI transport, may be given either orally or by retention enema (the rectal route works more quickly). Administered with ginger ale or diluted with D5W or NSS to help prevent gastric ulceration.
d. Dialysis may be indicated as it is the most effective treatment.
e. The nurse must monitor the patient’s ECG continuously and lab values hourly.
how to treat high phosphate 3
Serum phosphorous and calcium are usually in inverse relationship. If calcium levels are low, phosphorous levels will be elevated
a. Don’t eat high phosphate foods (sardines, organ meat, dairy, dark sodas)
b. Adequate hydration
c. Phosphate binders WITH meals
2 ways to tx acidosis in aki
acidosis may occur because of kidneys inability to secrete hydrogen
- If patient can compensate with increasing respirations then do not intervene
- If confused, hyperactive reflexes, tingling, tetany, seizures, ph <7.2, HCO3 <15 – this means metabolic acidosis and must give Na bicarb
*most effective is dialysis if severe acidosis
3 nutritional support in aki
- The goal of nutritional support in AKI is to maintain ideal body weight, albumin level 3.5-4 g/dL, total protein 6-8 g/dL, and normalize electrolytes.
- Adequate nutrition is important to support immune system function, prevent/treat protein-energy wasting and metabolic complications, and reduce mortality.
- Oral or enteral nutrition is preferred to parental nutrition.
3 comfort measures of aki
- Sources of discomfort in patients with AKI include thirst due to fluid restriction, pruritis due to high levels of urea from high BUN levels, pain due to invasive lines, and anxiety due to severity of illness.
- Pruritis can be helped by keeping skin moist and cool, using tepid water to bathe the patient, applying Stiefel Sarna anti-itching lotion, and administration of a H1 receptor antagonist.
- Appropriate education and explanations based on patient and family needs may help reduce anxiety.
how to prevent complications of aki
hand hygiene, strict aseptic technique in care of invasive devices, limiting the use of indwelling catheters, utilizing ‘bundles’ to reduce ventilator-associated pneumonia in intubated, ventilated patients, monitoring the patient’s temperature and CBC, and collecting specimens if infection is suspected.
tx of removal of nitrogenous waste in aki
- Both BUN and creatinine rise as GFR decreases in AKI. Azotemia (BUN > 90-100) occurs when there is an accumulation of nitrogenous waste in the blood and is a clinical characteristic of uremia.
- Uremia occurs when creatinine clearance is below 10-20 mL/minute. The patient may have the following symptoms – mental status changes, visual disturbances, anorexia, nausea, vomiting, pruritus, pericardial friction rub due to uremic pericarditis, muscle cramps, increased thirst, hypertension, fluid overload, metabolic acidosis, and electrolyte imbalances.
- Dialysis or renal replacement therapy (RRT) should be initiated when these symptoms are present and not treatable by other methods.
diffusion
solutes move across a semipermeable membrane from a solution where they are in higher concentration (plasma) to a solution of lower concentration (dialysate). The amount of solute removed depends on dialysate flow rate and duration of treatment.
osmosis
a solution (H2O) moves from an area of low solute concentration (plasma) to an area of higher solute concentration (the dialysate).
ultrafiltration
a pressure gradient is created between the sides of the semipermeable membrane. The rate of ultrafiltration depends on the porosity of the membrane and the hydrostatic pressure of the blood (which is dependent on blood flow). The faster the flow, the larger the solute can be carried.
how does intermit dialysis work, when to use intermit dialysis
- long term, lower cost , intense and effective quickly
-uses both ultrafiltration and diffusion to rapidly correct electrolyte imbalances, restore fluid balance, and remove wastes.
- indicated in patients with severe fluid overload and electrolyte imbalances, AKI, high creatinine but stable BP or chronic renal failure, certain types of drug overdoses or poisoning, and transfusion reactions.
when is CRRT used
short term , more cost and VERY labor intensive, slow continuous, less intense
complications of intermit dialysis
rapid shifts in plasma volume leading to hypotension, arrhythmias due to rapid shifts in electrolytes, difficulties with vascular access, and dialysis disequilibrium syndrome.
7 nursing actions for CRRT
- Labs drawn before treatment and during: electrolytes, BUN, creatinine, glucose, CBC, PT/PTT
- Assess and maintain access
- requires anticoagulation (usually heparin, although citrate can be used) so PREVENT bleeding
- Aseptic care to prevent infection
- Monitoring and maintaining normal body temperature
- Monitoring I & O (every 30 minutes-hourly)
- Frequent assessment of vital signs
when can pt be weaned from CRRT
when spontaneous urine output is > 400 mL/day.
normal RBC
3-5
normal hgb
13-16 male
11-15 female
normal WBC
4500-11000
normal platlets
150k, 450k
normal BUN
6-20
normal CO2
23-29
normal Creatiine
0.8-1.2
normal glucose
64-100
normal chloride
normal Na
136-144
normal Ca
8.5-10.2
normal prothombin time
11-15 sec
normal inr
0.9-1.3
normal aptt
25-40 sec
normal thrombin time
<24 sec
normal fibrinogen
1.5-4.5
normal lactate
< 2
