Exam 2 Flashcards
what is ventilation
the movement of air btw atmosphere and the alveoli-by inhalation/exhalation, higher to lower pressure
minute ventilation
volume inhaled/exhaled per minute = 7500ml at rest
alveolar ventilation
volume of fresh gas entering respiratory zone available for gas exchange per minute
if rapid breathing, how are PaCO2 and alveolar ventilation impacted
alveolar vent is increased and CO2 decreases
diffusion
exchange of O2 and CO2 b/w pulmonary capillaries and the alveoli
what impacts diffusion (4)
- Affected by surface area available for diffusion
- Affected by thickness of alveolar-cap membrane
- partial pressure of gas across the membrane
- and solubility and molecuar characteristics of the gas
perfusion
flow of blood through the pulmonary capillary bed
what is transport
Oxygen and co2 being circulated in the blood and to and from the cells
how is o2 transported
RBCs - hemoglobin (97%)
Dissolved in blood (3%)
how is co2 transported
Dissolved in blood (10%)
Attached to hemoglobin (30%)
Bicarbonate in bloodstream (60%)
What drugs can go down ET tube because they are metabolized in lung tissue?
Lidocaine
Epi
NARCAN
Atropine
conducting airways
No actual gas exchange takes place here (anatomic dead space)
Nasopharynx warms, humidifies and filters air
Includes naso and oropharynx, trachea, bronchi, bronchioles, and terminal bronchioles
respiratory airways
Respiratory bronchioles, alveolar ducts, and alveolar sacs
Surrounded by smooth muscle
type 1 alveolar cells
responsible for gas exchange
type 2 alveolar cells
secrete surfactant
Macrophages present to remove foreign substances
what is the v/q relationship
Ventilation/perfusion (V/Q) relationship
Measure of how well someone is ventilating vs perfusing
what is the normal v/q
Normal is 0.8 - 1 (4L/minute of ventilation to 5L / minute of perfusion)
what 5 things influence V/Q
- anatomical dead space
- alveolar dead space
- anatomical shunt
- physiological shunt
- silent unit
anatomical dead space
Conducting airways
*Tubing from ET tube back to ventilator - adds dead space
High V/Q ratio (alveolar dead space)
-Normal or good ventilation with decreased or no perfusion
-When regions in respiratory airways are ventilated but not perfused
-ex: pulmonary embolism, cardiogenic shock (amount of o2 in alveoli is so low)
shunt
blood bypasses alveoli w/o picking up O2
anatomical shunt
Patent ductus arteriosus
ASD
VSD
Patent foramen ovale
Mixing of oxygenated and deoxygenated blood → dilutes oxygen to tissue
physiological shunt (low VQ)
low ventilation, normal perfusion
decreased gas exchange
d/t obstruction like a mucus plug in the tube
physiological shunt (high VQ)
High VQ (good ventilation) but poor perfusion = alveolar dead space
I.e. PE, cardiogenic shock
silent unit
low / no perfusion and low/no ventilation
(ex: pneumothorax, patient with ARDs)
normal PaO2: FiO2
normal > 300
what does a PaO2: FiO2 of 200-300 mean
one of the mismatches is happening → 15 - 20% shunting
what does a PaO2:FiO2 of 100 mean?
100 > 20 % shunting
four cardinal symptoms of respiratory distress
Dyspnea
Chest pain
Sputum production
Cough
crackles
rales - high pitched brief popping sound heard during inspiration
Fluid in smaller airways / alveoli trying to open and not opening or terminal airways that are collapsed
Classic in CHF, pneumonia
Sounds like hair being rubbed together
rhonchi
Deep low pitched rumbling
Snore, gurgle
Can be expectorated
Noise comes from sputum in airways
Bronchitis, pneumonia
wheeze
Asthma, COPD
High pitched
friction rub
Same as pericardial rub
Usually heard on inspiration
Two surfaces with fluid are rubbing together
Sounds like sandpaper
Hear in heart beat - pericardial effusion
Cardiac or respiratory?
Would go with rate - either HR or RR
stridor
High pitched inspiratory sound
Crowing
When we have air passing through constricted trachea
Constriction, obstruction
Medical emergency
Need to be intubated or intubated
Croup in pediatrics
3 goals of O2 therapy
Correct hypoxemia
Decrease work of breathing
Decrease myocardial workload
if you patient has a problem with oxygenation, what do they need
more FiO2
if your patient has a problem with ventilation, what do they need
more flow (bipap, cpap or additional breaths)
what is effective O2 therapy
lowest FiO2 and lowest amount of oxygen - to achieve normal SaO2 or normal PaO2 on pulse ox
6 factors affecting success of supplemental O2
medical history
LOC
patent airway
RR
depth of breathing (tidal volume)
hgb level
5 complications of supplemental o2
Skin breakdown
Drying of mucous membranes
Epistaxis
Infection of the sinuses
Oxygen toxicity
who can get CPAP
Can only be used on patients breathing spontaneously - just o2 issues, not ventilation issues
5As for treating smoking use and dependence
Ask about tobacco use - at every visit
Advise to quit
Assess willingness to make attempt to quit
Assist in attempt at quitting - offer medication, provide counseling or referral
Arrange follow up
pulmonary function test
Measures lungs ability to move air in and out of alveoli
CT scan (PE protocol)
Need large bore IV, know kidney functions
Contrast - hold metformin for 48 hours after to avoid lactic acidosis
Check lab results
*Contrast dye is nephrotoxic
what can a chest x ray be used for
Sees tubes/drains/catheter placements
Pulmonary edema, pleural effusion
pneumothorax
Can see bones
See infiltrates
Cardiomegaly → muscle has gotten thicker/hypertrophied → means EF is low
bronchoscopy
direct visualization of tracheobronchial tree/larynx
Can remove foreign objects
Can do biopsies
Can stop bleeding
Can be done while patient is ventilated
thoracentesis
Can remove fluid during pleural effusion → decreased surface area for o2 and co2 exchange → SOB, DOE
Can be diagnostic or therapeutic
Therapeutic = symptom mgmt
Diagnostic - send drainage to lab and get diagnosis - (i.e. WBC, cancer cells, etc)
end tidal co2 monitoring
Measures maximal partial pressure of CO2 obtained at the end of an exhaled breath
capnography
continuously monitors the PaCO2 in the airway during inhalation and exhalation and provides a written tracing
normal paCO2 values
35-45 mmhg
normal HCO3 - values
22-26 meq/l
normal PaO2
80-100 mm hg
what is an anion gap and what is the normal level
specialized blood tests that lets us know about metabolic acidosis
Look at difference b/w sodium + potassium on one side and Cl and HCO3 on the other
Less than 12 = normal
BNP
Want to know if someone has pulmonary edema d/t HF → will impact oxygenation
Increases as HF worsens
normal BNP level
less than 100
BNP of 100-300
mild volume overload of some kind
BNP of over 600
moderate HF, pulmonary edema
BNP of over 1000
severe pulmonary edema
BNP over 5000
kidney problems
D Dimer and normal level
indicates Degradation of certain fibrin molecules in the blood
Normal = less than 0.50
what meds are important with COPD exacerbation (4)
Bronchodilators, mucolytics, corticosteroids, oxygen
what meds are important with pulmonary edema?
diuretics, oxygen
which med is most important with CHF or pulmonary edema
diuretics
how to get ABG sampling
-Radial, brachial or femoral site (no tourniquet needed)
-Wipe with chlorhexidine, 20G needle, heparinized syringes, insert 30 - 45 degrees with bevel up right below where you feel the pulse → 3-5ml → hold pressure for 3-5 minutes on artery → put sample it on ice and to the lab (ice to reduce oxygen metabolism and give more accurate reading)
allen’s test
if using radial approach for ABG sampling
Testing patency of other vessel supplying hand - ulnar artery
Positive test = ulnar is patent
uncompensated ABGs
ph and 1 PaCO2 OR HCO3- are going to be abnormal
partially compensated ABGs
ph is still abnormal and both PaCO2 and HCO3 are abnormal
fully compensated ABGs
ph is normal but PaCO2 and HCO3 are not normal
indication for chest tubes
To drain fluid or air from the thoracic cavity, in the pleural space
-Hemothorax
-Pneumothorax
-Tension pneumothorax
-Pleural effusion
hemothorax
Blood collects b/w chest wall and lungs in pleural cavity
Can cause lung to collapse if volume buildup is so high
s/s of hemothorax (4)
Chest pain
Difficulty breathing
Reduced breath sounds on affected side
Rapid heart rate
pneumothorax
Air leaks into space b/w lung and chest wall
can be closed, open or tension
tension pneumothorax
air in pleural space increasing and unable to escape
Pressure is so great that lung pushes up and becomes non functioning
Everything is pushed (trachea, heart) to unaffected side
Breath sounds will be absent on affected side
tx for tension pneumothorax
needle decompression w/ large bore needle into 2nd intercostal space in midclavicular line
pleural effusion
Fluid between pleural space, 2 pleural linings
s/s of pleural effusion
SOB,
chest pain especially when breathing in deeply,
activity intolerance,
DOE,
cough
tx for pleural effusion
drained with thoracentesis or chest tube
3 chambers of drainage systems for chest tubes
Collection
Water seal chamber
Suction apparatus
what is normal finding in drainage system
Tidaling - normal finding subtle up and down of water in under water seal chamber (usually middle chamber)
normal finding in chest tube drainage system for spontaneous breathers
Should rise a little with inspiration because you are getting more negative
Should fall during expiration when patient is breathing spontaneously
normal finding in chest tube drainage system for mechanical ventilation
Fall during inspiration because you are putting positive pressure into lungs
Should rise during expiration when positive pressure is pumped out
how often do you check VS and CV/pulm for patient with chest tube
q2
how often do you mark and monitor drainage for chest tubes
q15, q 30, q1, q4,q8
what does a sudden increase in drainage mean?
could be internal bleeding
More than 150-200 ml when its been going down → need to let someone know
what does it mean if the chest tubes suddenly stop draining
expect its a clot
assess for air leaks and that connections are sealed
how will patient breathe with chest tube
they’ll be in pain so more shallow breathing –> can lead to atelectasis
pt should splint with pillow towel and be medicated
subq emphysema
When you palpate - feels like rice krispies = air is escaping from lungs
Happens if chest tube moves → air will escape into sub q tissue
Looks like edema
Long time to reabsorb back in
what is another complication of chest tubes
tension pneumo
what do you do if there is a dislodgement or accidental removal of chest tube
Petroleum gauze with DSD and occlusive tape: occludes the opening
paO2
Measures oxygen levels in arterial blood
No acid base role
Indicates hypoxemia when low
SaO2
Represents % of hemoglobin molecules that are bound with O2 in arterial blood
normal level of SaO2
93-97%
what can cause resp acidosis
May be result of inefficient pulmonary function or excessive production of CO2
CNS depression
Decreased ventilation
Pulmonary edema
causes of resp alkalosis (6)
Anxiety
Fear
Hypoxia
Pain
Head injury
Mechanical ventilation
causes of metabolic acidosis (4)
Diarrhea
GI losses
Renal failure
DKA / ketoacidosis (Ketones are produced when body is forced to use fat to create injury because lack of insulin that is converting glucose to energy
Fat is turned into ketones = acids → accumulate in bloodstream)
causes of metabolic alkalosis (4)
Vomiting
Diuretics
High NG output
Antacids
what is the normal amount of drainage in the drainage system
typically less than 100 cc/hr
what does excessive bubbling in the air leak monitor mean
can mean air leak
what does intermittent bubbling in the air leak monitor mean
pt might have pneumothorax (expected)
if chest tube becomes dislodge, what do you do?
Sterile dressing
Tape on 3 sides - allows air to escape and prevent pneumo
Notify MD
steps for chest tube removal
-Done at bedside by physician
-Gather supplies - sterile gloves, suture removal kit
-Teach valsalva’s maneuver - deep breath, exhale and bear down during removal – prevents air entering pleural space during removal
-Pre-medicate for pain
-Position semi fowler’s
-Monitor respiratory status, lung sounds, drainage, chest rising, dyspnea
-chest x ray to assess lung
6 goals of intubation
-Maintain alveolar ventilation appropriate for the patient’s respiratory & metabolic needs
-Correct hypoxemia and maximize oxygen transport
-Protect the airway
-Alleviate respiratory distress
-Prevent or reverse atelectasis
-Acid/base balance
indications for intubation
-Brain injury
-Surgeries b/c of general anesthesia
-Airway obstructions
-Non-patent airway d/t trauma
-V/Q mismatch (PE, Pneumothorax)
-Copious amounts of secretions
-Prevention for aspiration and pneumonia
-coma
-change in LOC
-impending cardiac arrest
what flow should ambu bag be set at during intubation
15 L flow, 100% oxygen
nurse’s role pre-intubation (10)
-Vitals, O2 sat
-Consent if elective
-Allergies
-Know history
-Labs
-Pre-medications
-Ambu bag - provide oxygen
-Gather equipment
-oxygenate/ventilate the patient
-Suction PRN
nurse’s role during intubation
-Vitals
-Auscultate breath sounds bilaterally
-Timing procedure → don’t want patient going too long without o2
-Inflate cuff
-Secure tubes
-Bag until vent arrives
-Order CXR
-Note tube placement
meds for intubation: neuromuscular blockers or sedation first
sedation
sedation meds (3)
Etomidate
Propofol
Midazolam (Versed)
neuromuscular blockers (4)
Succinylcholine (agonist)
Vecuronium (antagonist)
Rocuronium
Pancuronium
how to confirm placement of intubation
-Bilateral breath sounds
-Colormetric CO2 detector - Gold is good
-Misting in the tube
-CXR to confirm placement
-Capnography waveform reading
-End tidal co2
cuff management following intubation (pressure number, how often to check, what’s the purpose)
To prevent trachea ischemia, fistulas - use low pressure high volume cuff
Don’t want above 20-25 mm Hg pressure
Should check q8h
nursing mgmt of tube: suctioning
Sterile procedure
In line or catheter
Pre-oxygenate FiO2 100% 3x then suction
Do not suction for more than 15 seconds
No more than 3 passes at a time
oxygen/FiO2 mgmt for patients with tube
Usually started on 100%
Usually titrated to maintain PaO2 > 60 mmHg (SaO2 > 90 mmHg)
when are patients at risk for oxygen toxicity
FiO2 60% for more than 24 hours
how do you know if you can turn down patients oxygen levels with tube
ABGs
minute ventilation
RR x Tidal Volume –> determines alveolar ventilation
what is tidal volume
volume of gas (ml) delivered/ moved in/out of lung in a normal inspiration/expiration
normal tidal volume
5-8 ml/kg
what is lung protective tidal volume levels
6-8 ml/kg
what is PEEP
Positive End Expiratory Pressure
Positive pressure delivered at end of expiration to keep alveoli open
what level of PEEP is adequate in most patients to maintain SaO2 or PaO2
Low pressures (2-5cm H2O)
what PEEP pressure do patients with refractory hypoxemia (ARDs) get
8-10 cm H2O
complications of PEEP
-impedes venous return –>
decreases CO and BP
-decreased circulatory flow
-hypotension
high pressure alarm
indicates increases airway resistance or decreased lung compliance
Decreased lung compliance d/t atelectasis, pneumothorax, pulmonary fibrosis, pulmonary edema
Increased airway resistance d/t bronchospasm, bucking the ventilator, coughing, secretions, biting, kinks, agitation
low pressure alarm
d/t disconnection
what should do if alarm is going off
ventilate with Ambu bag until you figure it out
ET tube complications
-Oral vs. Nasal
-Lip, tongue, teeth, tracheal damage
-Mucous plugs
-Patient bites tube
-Sinusitis
-Fistula
-Granulomas
-Infection- VAP
-Cuff ulceration
how to prevent aspiration
OG tube
Head elevation > 30
Suction
Cuff pressure - 20-24 mm Hg
what does aspiration increase risk of
VAP or ARDs
barotrauma
rupture of alveoli or emphysematous bleb secondary to the increased positive pressure (with ventilation/PEEP) which leads to air tramping in pleural space and development of Tension Pneumothorax = medical emergency!
VAP
Second most common HAI
Pt who has been intubated for at least 48 hours
Will appear white on CXR
nursing prevention measures for VAP
Hand washing
Gloves while manipulating or suctioning ETT
VAP bundle
-Oral care q4h
-HOB 30-45 degrees
-GI prophylaxis w/ PPI
-DVT prophylaxis w/ lovenox (40 ml sq daily = preventative)
-OOB
-Alcohol free mouthwash, teeth brushing, frequent oral suctioning
what is a bundle
Bundle = intervention with 4-6 related interventions - done together decreases issue
criteria for weaning
Hemodynamically stable
Core temp > 36, < 39
Cxray-no abnormal findings, treat pathology prior
SaO2 > 90% on FiO2 of < 40% and PEEP of 5 or less
ABG and major electrolytes WNL or baseline for patient
No residual paralytics
Hematocrit > 25%
Adequate pain/anxiety/agitation management
patient positioning during weaning trials or removal of ET tube
reverse trendelenburg and/or semi- to high-Fowler’s position may improve respiratory movements
ARDs
Considered a complex syndrome
Inflammatory lung injury resulting in HYPOXEMIA
Many different causes but all involve some sort of direct or indirect injury to the lung
*diagnosis of exclusion
most common cause of ARDs
sepsis
Berlin definition ARDs: oxygenation mild
200 mg Hg < PaO2/FiO2 <= 300 mm Hg with PEEP or CPAP >= 5cm H2O
Berlin definition ARDs: oxygenation moderate
100 mm Hg < PaO2/FiO2 <= 200 mm Hg with PEEP >= 5cm H2O
Berlin definition ARDs: oxygenation severe
PaO2 / FiO2 <= 100 mm Hg w/ PEEP >= 5cm H2O
criteria of Systemic inflammatory response syndrome (SIRS)
two or more of the below:
Temp > 100.4 F or < 98 F
Heart rate > 90 BPM
Respiratory rate > 20/min or PaCO2 <32 mm Hg
White Blood Cell count >12,000 cells/mm3 or < 4000 cells/mm3 or > 10% immature (band) forms
what is SIRS
Systemic inflammatory response syndrome
can lead to multisystem organ dysfunction with the respiratory system usually being the first affected
what do the stages of ARDS respresent
symptom onset progression
ARDs stage 1
first 24 hours
Subtle sign = tachypnea
-restlessness,
-dyspnea
-moderate to extensive use of accessory muscles
-No changes on xray yet
-ABG may show resp alkalosis
ARDs stage 2
24-48 hours
s/s: tachypnea, dyspnea on exertion, tachycardia, use accessory muscles, agitated/confused b/c of hypoxia
Coarse bilateral crackles
Decreased air entry into dependent lung fields
CXR: patchy bilateral infiltrates
ABG decreased SaO2 despite supplemental O2
ARDs stage 3
2-10th day
-Crackles in lungs → white out lungs
-Increased lethargy
-Change in LOC
-O2 sat decreasing, Need more O2
-Increase in arrhythmias, chest pain
-CXR: decrease lung volumes
-Renal system affected - decreased output, edema
-decreased bowel sounds
-ABG: worsening hypoxemia
ARDs stage 4
after 10 days
-Symptoms of MODS
-CXR: Pneumothoraces pneumos
-Surfactant damaged causing alveolar collapse
-ABG Worsening hypoxemia and hypercapnia (more shunting now)
ARDs late symptoms (b/w stages 3-4)
need to be intubated, high FiO2 %, high PEEP, diffuse crackles, tachycardic with decreased CO, hypotension, might need vasopressors for BP, might need CCRT to filter blood
3 pathophys hallmarks of ARDs:
Change in lung vascular tissue
Increase in lung edema
Impaired gas exchange
oxygenation goals for ARDs
PaO2 of 55-88 mmHG with SaO2 88-95%
PaO2: FiO2 ratio goal for ARDs
200-300
secondary complications of ARDs
Ventilator assisted/induced lung injury (VALI/VILI) - Barotrauma, volutrauma
SIRS
Multisystem organ dysfunction (MODS) due to hypoxemia
PE, DVT, atelectasis, and nosocomial infections due to immobility
acute respiratory failure
Characterized by sudden and life threatening deterioration of gas exchange
Results in CO2 retention (hypercapnia) and/or inadequate oxygenation (hypoxemia)
Acute respiratory failure PaO2
< 55- 60 mm Hg hypoxemia
acute respiratory failure PaCO2
> 50 mmHg hypercapnia
acute respiratory failure ph
< 7.35 severe acidosis
two classifcations of acute respiratory failure
- acute hypoxemic respiratory failure
2 acute hypercapnic respiratory failrue
Acute Hypoxemic Respiratory Failure
Defect in oxygenation
PaO2 of < 55-60mmHg
acute hypercapnic respiratory failure
Defect in ventilation
CO2 > 50mmHg
r/t ventilation side - decreased ventilatory drive (narcotics, alcohol, brainstem lesion, ALS, increased work of breathing d/t COPD exacerbation or asthma)
diagnostics for acute respiratory failure
ABGs
CXray for opacities to see if it is pulmonary edema
nursing mgmt for acute respiratory failure
-Airway: intubate and ventilate
-O2: restore and maintain oxygenation - 100% while waiting for intubation
-Correct Acid-Base disturbance with ventilator support
-Restore Fluid/electrolyte balance - might need diuretics
-Optimize cardiac output w/ PA catheter
-Nutritional support
-Treat underlying cause
(I.e. pneumonia → antibiotics
Volume overload → diuretics)
if it is determined that acute respiratory failure is a ventilation problem, what do you do
ambu bag, narcan, give more breaths, stop sedation
if it is determined that acute respiratory failure is a oxygen problem, what do you do
give more O2
what is the number one answer to increase perfusion
IV fluids
how to assess perfusion
cap refill
> 3 is not good
acute respiratory failure goals
-Patent airway will be maintained
-Oxygenation will be maintained: PaO2 of 80-100 mmHg with SaO2 > 90%
-ABGs will be within normal limits
will hypoventilation increase or decrease ETCO2
increase
with each cardiac cycle, what % of CO is pumped into kidneys
20%
1.2 L/minute
what is urea
breakdown of protein
what is creatinine
end product of breakdown of muscle
RAAS system
Decreased BP d/t dehydration or blood loss → renin released → angiotensinogen converted to Ang I converted to ang II w/ ACE → a2 constricts smooth muscle of arterioles → increased BP → increases GFR
how does ADH work
chemical produced in the brain that causes the kidneys to release less water, decreasing the amount of urine produced
aldosterone
secreted when GFR falls and increases Na+ & H2O reabsorption → increases GFR
ACE inhibitors
Prevents conversion of Angiotensin 1 to angiotensin 2
Stops Na secretion, stops ADH production, stops arteriolar vasoconstriction
ARBs
Blocks receptors thereby promoting vasodilation, Na and H2O excretion
spironoloactone
Works in late distal convoluted tubule to prevent reabsorption of Na
Potassium sparing
least amount of diuresis
furosemide
loop diuretic
Prevent reabsorption of Na and K in ascending loop of henle
*most diuresis
HCTZ - hydrochlorothiazide
thiazide diuretic
Prevents Na reabsorption in early distal convoluted tubule
first line for HTN
how do we measure kidney function
GFR
GFR
Measure of filtration efficiency based on Cr in serum
normal GFR
> 60
if BP is low, how does smooth muscle in kidneys react
BP is low - smooth muscle will vasodilate → increase perfusion to keep GFR constant
if BP is high, how does smooth muscle in kidneys react
If BP is high → smooth muscle will vasoconstriction to decrease perfusion to keep GFR constant
renal blood flow path
Receives blood from renal artery → branches into afferent arteriole → capillaries / glomerulus → filtration → leaves by efferent arteriole
two biggest risk factors for kidney failure
HTN and diabetes
how will lung sounds when volume is up
crackles or wheezes
What can skin tell you about kidneys
-Bruising and bleeding - low H&H
-Tenting - shows dehydration
-Dry itchy skin
-Uremic frost - uric acid deposits in skin if not excreted
CVA tenderness
back pain
can indicate infection
*check temp
thrill
palpable pulsation of AV fistula or graft
bruit
a functional AV fistula or graft has a a bruit on auscultation
if you don’t hear a bruit or feel a thrill
AV fistula has clotted off = medical emergency
What Review Of Systems questions are important for kidney fxn?
Urine output
Abdominal pain
n/v
Back pain
Rashes, itching
Lower extremity edema
SOB
Fever
if urine is cloudy, what is that a sign of
infection
if urine is clear/colorless, what is that a sign of
diuretics
what should not be in urine
Proteinuria, blood, WBC, LE, Nitrites, casts, or glucose
if UA is + for WBC, nitrite, leukesterase, what does that indicate
UTI
can empirically start antibiotics
what will hyperkalemia look like on EKG
T wave will be higher than QRS
how to tx hyperkalemia
Tx: IV D50 then regular insulin
Tx: calcium gluconate, sodium polystyrene sulfonate (Kayexalate)
Tx: dialysis
Chvostek’s sign
hypocalcemia
Trousseau’s sign
hypocalcemia, hypomagnesimia, and metabolic alkalosis
what is a sign of hyponatremia
look for neuro disturbance can be anything from lethargy to seizure to coma, the lower it is < 135, < 120 is very bad, <116 is probably having major neuro disturbance-confusion, seizures
normal cr level
0.6-1.2 mg/dl
normal bun level
8-20 mg/dl
when will BUN increase out of proportion to Cr
If patient is volume depleted, dehydrated or internal bleeding
azotemia
BUN/Cr are both elevated
KUB XR
kidney, ureter, bladder
can see stones, size of kidneys and hydronephrosis
kidney radiology options
KUB XR
CT abdomen/pelvis
MRI
pyelogram
renal or renal artery US
kidney biopsy
what will renal US show
Best for renal artery stenosis
What happens to RAAS in renal artery stenosis → messes with BP, harder to control
Can see obstructions in systems
what do you want to check for after kidney biopsy
bleeding
AKI
Abrupt or rapid decline in renal filtration function - seen w/ decreased GFR
Cr will double with 50% decrease in GFR
risk factors for AKI
Older adults
Diabetics
Chronic kidney dysfunction
Chronic heart and liver disease
causes of prerenal AKI
-Decreased CO → decreased perfusion to kidneys
-Hypovolemia
-Shock states
-Excessive diuresis (meds or hyperglycemia)
how to tx prerenal AKI
Treat underlying cause
IVF, pressers, inotropes
Can be reversible with early intervention
what is a sign of a AKI in older adults
change in mental status
cause of intrarenal/intrinsic AKI
d/t acute damage of the glomeruli, renal parenchyma
-ATN (acute tubular necrosis)
Ischemic, Toxic (aka contrast dye, some antibiotics), Most common
-AIN (acute interstitial nephritis)
-GN (glomerulonephritis)
-Prolonged hypoperfusion
-Rhabdomyolysis
-Malignant HTN
-Kidney transplant rejection
-Infections
s/s of intrarenal AKI
Hematuria, lower extremity edema, HTN if glomerular issue
intrarenal/intrinsic AKI tx
Stop nephrotoxic meds
Hydrate
Treat underlying chronic diseases
post renal AKI causes
d/t damage / obstruction along the urinary tract system - obstruction of flow from collecting ducts to external urethral orifice
Causes:
Cellular debris
Kidney stone
Tumor
Prostate enlargement
Trauma to the urinary tract
Renal vein thrombosis
how to tx post renal AKI
remove obstruction, foley to empty bladder
incidence of intrarenal/intrinsic AKIs
up to 40% of all AKI cases
incidence of prerenal AKIs
As many of 21% of inpatient AKI
incidence of post renal AKI
Lowest incidence of all AKI cases - 10%
what is the most common cause of renal failure
acute tubular necrosis
causes of ATN
Nephrotoxic drugs
-Damage to epithelial layer
-Antibiotics
-Contrast media
-Heavy metals
-Environmental chemicals
Ischemic origin
-Basement membrane origin
-Hypovolemia
-Decreased CO
-Systemic vasodilation
-DIC
-Renal vasoconstriction
nephrotoxins
NSAIDs
Lithium
Benadryl, doxylamine
Acyclovir
Aminoglycosides
Amphotericin
Quinolones
Rifampin
Sulfonamides
Vancomycin
Antiretrovirals
Cyclosporine, tacrolimus
ACEs/ARBs
Chemotherapeutics
Contrast dye
Loop/thiazide diuretics
what GFR indicates CKD
GFR < 60 for 3 months or greater
Glomerulosclerosis
scarring of the filtering part of the kidneys (glomerulus)
Can be d/t diabetic nephropathy or hypertensive nephrosclerosis
risks for CKD (5)
DM
Age
HTN
AKI
High cholesterol
is CKD reversible?
no - pregressive and irrreversible
how to tx CKD
Monitor labs
Avoid nephrotoxic drugs
Encourage PO hydration
ACE and ARB is renal protective in early disease
Mange comorbid conditions
prognosis of CKD
CKD is a comorbid condition and increases in hospital morbidity and mortality rates
May progress to ESRD if left untreated
what GFR indicates renal failure
GFR < 15 on dialysis
AEIOU: emergent need for RRT
A - intractable acidosis
Ph < 7.2 or 7.3
E - electrolyte imbalance (hyperkalemia) and not responding to kalexylate or IV insulin
I - intoxicants (methanol ethylene glycol, Li, aspirin)
O - intractable fluid overload
U - uremic symptoms (nausea, seizure, pericarditis, bleeding)
AV fistula
surgical anastomosis of an artery and a vein
AV graft
created by inserting a prosthetic graft between an artery and vein, typically in the nondominant arm.
*not preferred, doesn’t last as long as fistula
AE of hemodialysis
hypotension
if patient is hypotensive during or after hemodialysis, what should the nurse do
stop dialysis, check vitals, call provider
Hemodialysis Teaching & Complications
Cannot miss a dialysis treatment
Signs of infection
Hemorrhage from dialysis access
Aneurysm or pseudoaneurysm of access
Hypotension/hypertension from fluid imbalance
Thrombosis of dialysis access
signs of peritonitis and tx
Cloudy drainage
Low grade temp
Abdominal pain
Tx: broad spectrum antibiotics
what does retained dialysate indicate and what should you do?
Should drain equal or more than put in to dwell
Check tubing, reposition patient, lower the drainage bag, assess for s/s of fluid overload, fullness, or discomfort
what is CCRT
continuous renal replacement therapy
Reserved for patients too unstable for HD
Hemodynamically unstable patients
Continuous slow filtration
AE of CRRT
hypotension
hypothermia
does HD or CRRT remove more blood
HD
what does Blood streaked sputum indicate
carcinoma of the lungs
what must be done when you change vent settings
draw ABGs within 20-30 minutes
3 signs of o2 toxicity
collapsing of alveoli
seizures
disorientation
aspiration can increase risk of which 2 resp illnesses
VAP (pneumonia) and ARDS
how to decrease risk of aspiration (4)
OG tube
Head elevation > 30
Suction
Cuff pressure - 20-24 mm Hg
4 criteria for ARDs
timing (w/i 1 week of known insult or worsening of respiratory symptoms)
chest imaging
origin of edema
oxygenation
3 pathophys hallmarks of ARDS
Change in lung vascular tissue
Increased lung edema
Impaired gas exchange
VAP bundle
-Oral care q4h
-HOB 30-45 degrees
-GI prophylaxis w/ PPI
-DVT prophylaxis w/ lovenox (40 ml sq daily = preventative)
-OOB
-Alcohol free mouthwash, teeth brushing, frequent oral suctioning
A patient with a chest tube has no fluctuation of water in the water seal chamber. What could be the cause of this?
The lung may have re-expanded or there is a kink in the system
How many RR do you start someone with on a vent?
10-12 breaths/minute
Functions of kidneys
Filtration & excretion
Electrolyte, fluid, acid/base balance
BP regulation
RBC production stimulation
Regulate calcium reabsorption in the bone
s/s of tension pneumo
hypotension, hypoxia, breath sounds absent on affected side
