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154 Cards in this Set
- Front
- Back
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Low V/Q ratio
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less than .8
Pt has low ventilation, perfusion is normal |
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High V/Q ratio
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normal ventilation, low perfusion
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Very low V/Q
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shunting, blood is leaving lungs completely unoxygenated
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Normal Tidal Volume
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500 mL or 5-7 mL/kg
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Acute Respiratory Failure
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- PaO2 less than 60 mmHg
- PaCo2 greater than 50 mm Hg - pH less than or equal to 7.30 |
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Etiology of Respiratory Failure
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- failure of oxygenation
- Failure of ventilation - both of the above (Pneumonia, HF) |
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5 mechanisms that produce failure of oxygenation
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1. Hypoventilation
2. Intrapulmonary shunting 3. Ventilation-perfusion mismatch 4. Diffusion defects 5. Decreased barometric pressure (altitude) |
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Intrapulmonary shunting
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s large amount of blood returns to the left side of the heart unoxygenated leading to a decrease in PaO2
Decrease in ventilation and normal perfusion so blood is shunted past the lungs and returns unoxygenated to the left side of the heart |
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examples/causes of pulmonary shunting
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- atrial or ventricular septal defects
- atelectasis - pneumonia - pulmonary edema - pneumothorax, collapsed lung **oxygen will not help this because oxygen is not getting to where it needs to be |
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Most common cause of low O2
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V/Q mismatch
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Normal V/Q
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4:5 L/min
0.8 (book says 1) |
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Causes of Diffusion defects
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- fluid in alveoli
- Pulmonary fibrosis - changes in capillary pressure - leakage of plasma proteins into interstitial space - destruction of capillary membrane from fluid accumulation - lung fibrotic changes from COPD |
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Signs of Deffusion defect
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hypoxemia first affected
hypercapnia is a LATE sign |
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Earliest signs of respiratory failure
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neurologic (hypoxemia and hypercapnia)
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Main treatments for acute resp failure
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- maintain airway
- optimize o2 delivery - reduce o2 demands - treat the cause - prevent complication |
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ARDS criteria
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Non-cardiogenic pulmonary edema
- PaO2/FiO2 ratio less than 200 (basically giving o2 and seeing no results) - bilateral infiltrates - pulmonary capillary wedge pressure less than 18 mmHg (above this would be cardiogenic pulmonary edema) |
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Basic ARDS patho
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insult--> systemic inflammatory response syndrome (SIRS)--> inflammatory mediators--> damage to alveolar-capillary membrane--> increaed capillary permeability --> noncardiogenic pulmonary edema--> microatelectasis --> decreased lung compliance--> decreased surfactant--> imparied gas exchange (V/Q mismatch)
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early sign of ARDS
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hyperventilation (trying to blow off extra CO2 but won't work cause can't get it across membrane)
- may have respiratory alkalosis sat first and eventual metabolic acidosis - respiratory acidosis on ABGs eventually |
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Pros of Prone position in ARDS
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- alters V/Q ratio by shifting blood from posterior bases to anterior portion
- removes weight of heart and abdomen on lungs - increased removal of secretions - improves oxygenation - enhances recruitment of airways optimal duration is 18-23 hours daily, with therapy continuing until improvement of O2 is maximized * Can also do continual lateral rotation therapy |
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Complications of Prone position in ARDS
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- requires a lot of professional to move pt for safety
- don't dislodge ETT and other tubes and lines - gastric aspiration (turn tube feeding off for an hour before) - peripheral nerve injury (proper body alignment, careful arm positioning) - skin necrosis (pillow or foam supports, protective pads on shouldes, ileac crest, and knees) - corneal ulceration (lubricated and taped shut) - facial edema (moisture barrier applied to pts face to protect from mouth and nose drainage, basins, etc can also catch this) |
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COPD pt getting ARF
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- worsening V/Q mismatch (secretions, bronchoconstriction)
- can be caused by exacerbation, CHF, pulmonary edema, dysrhythmias (A fib becoming uncontrolled), pneumonia, dehydration, electrolyte imbalances **watch pH, this will show whehter it has become ARF or ARDS |
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Treatment of COPD pt with ARF
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- correct hypoxemia with CAUTIOUS O2 admin, noninvasive positive pressure ventilation (NPPV), ventilator assistance (avoid if possible, hard to extubate)
- Medications such as beta2 agonists, corticosteroids, and antibiotics if needed - cautious admin of sedatives- don't want to sedate ability to breath but want to reduce anxiety |
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Exacerbation of Asthma
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- wheezing
- dyspnea - chest tightness - cough (esp night time) - hyperventilation to reduce CO2 |
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Management of asthma exacerbation
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- oxygen and ventilation in severe cases (difficult to manage because spasm is low in lungs)
- IV corticosteroids - inhaled bronchodilators |
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4 things in asthma
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- bronchoconstriction
- airway edema - mucus plugging - airway remodeling |
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Asthma education
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- Environmental controls to prevent symptoms
- understand difference in meds - proper inhaler use - monitor asthma control - written action plan and goals |
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VAP prevention
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- handwashing and standard precautions
- aseptic suctioning of ETT - oral and nasal care - maintain ETT cuff pressure - elevate HOB - assess gastric residual volumes - turn and reposition frequently - oral care - extubate as soon as possible (sedation vacation and evals for this) |
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Treatment for VAP
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- bacteria- specific antibiotic therapy
- don't over use |
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Virchow's triad
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- venous stasis
- altered coag - damage to vessel wall (phlebitis) |
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Symptoms of PE
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- DVT
- chest pain worse on inspiration - dyspnea - tachy - cough, hemoptysis - crackles, wheezes - hypoxemia pt states "im going to die" |
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Prevention of PE
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- antiembolic hose
- SCDs - position changes - treatment of atrial dysrhythmias - prophylactic anticoag therapy |
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Surgical Treatment for PE
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- embolectomy
- vena cava umbrella (prevention) |
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Diagnosis of PE
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- clinical signs and symptoms
- chest xray to rule out other causes - V/Q scan with high probability of PE (nuclear medicine) - Pulmonary angiogram (Definitive!) - Spiral MRI/CT |
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Management of PE
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- ABCs, oxygen
- Thrombolytics - Heparin - Surgical procedures |
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pulse oximetry
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reflects the arterial oxygen saturation
- relation to Pa02 - less than 90% requires assessment |
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End tital Co2 (ETCO2)
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monitor ventilatory status. would be elevated in pts with respiratory problems
-must compare pulse ox and ETCO2 with ABGs for trending |
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Testing placement of endotracheal tube
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- Auscultate epigastric area
- Auscultate bilateral breath sounds - ETCO2 detector - chest xrays - 3-4 cm above carina |
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mechanical ventilation requires a _____ trach tube
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cuffed
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Indications for mechanical ventilation
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- Po2 less than 60
- PCO2 greater than 50 - pH less than 7.25 - PCO2 -PO2 - RR greater than 35/min - VT < 3.5 ml.Kg - VC< 15 ml/kg - NIF < -20 (like -5 or -10) - worsening chest xray - s/s of hypoxia |
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NIPPV (noninvasive positive pressure ventilation)
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- nasal CPAP or Bi-PAP
- to manage chronic or acute resp insufficiency |
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Positive pressure ventilation
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- requires artificial airway
- uses positive pressure to force air into lungs - adjustments to time, volume, and pressure |
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volume targeted ventilation
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set to allow air to flow to preset tidal volume
delivers TV regardless of compliance or resistance |
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pressure targeted ventilation
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- requires art airway
- air flows to pre set pressure - total volume will vary according to compliance and resistance |
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CMV- controlled mechanical ventilation
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- art airway
- preset total volume at a set RR - may be appropriate for pts unable to exert breath (ALS, SCI) * dysynchrony risk (pt brathing over vent) |
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Assist/Control (A/C)
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Vent will finish breath for pt and will breath for them if they don't breathe
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SIMV- Synchronized intermittent mandatory ventilation
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- preset tidal volume at preset RR
- premits pt to breath between at own rate and depth - good for weaning |
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Presure target mode
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- provides pressure during inspiration
- decreases work of breathing - presure support ventilation (PSV) |
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Positive end expiratory pressure (PEEP)
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- keeps airways open at end of expiration and increases FRC
- decreases FIO2 amount needed - risk for barotrauma and DECREASED cardiac output |
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CPAP (Continuous positive airway pressure)
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- augments FRC in spontaneous breaths
- vent or face mask in spontaneously breathing pts |
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mech vent nursing responsibilities
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- elevated bed 30-45 degrees
- sedation vacation daily - DVT prophy - peptic ulcer prophy - reposition ETT from side to side q 24 h - assess resp q 4h - monitor cuff pressure (20-30cm H20) - x-rays studies (serial) - secretions - pt hydration (if secretions are thick esp.) - monitor temp q 4h - oral care, hand washing - assess tolerance |
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Volutrauma =barotrauma
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lung injury or alveolar rupture (distention)
results in crepitus or pneumothorax caused by positive pressure vent, PEEP, high tidal volume |
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right mainstem intubation
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- assess for bilat chest excursion
- auscultate chest for bilat breath sounds - mark and assess tube position at tip |
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other intubation complications
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- endotracheal tube out of position
- unplanned extubation - tracheal damage - damage to oral or nasal mucosa - associated with o2 admin - blood gas abnormalities - aspiration - infections - vent dependence or inability to wean |
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LOW cardiac output
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- related to increased intrathoracic pressure
- PEEP |
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Neuromuscular blocking agents (NMBAs)
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paralytics
- use train-of-four (TOF)- goal is 2 out of 4 - succinylcholine (short acting) - curonium (long acting) **must be sedated also! |
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low volume alarm
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- pt does not receive preset tidal volume
causes: -disconnection, leak in cuff, tube out of position --> fix the cause |
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High pressure alarm
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- if preset pressure is exceeded
- secretions or mucous plugs - kinks in ET or tubing - biting - coughing and gagging - dysynchrony - barotrauma |
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Indications for Suctioning
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- by assessment
- visible secretions - frequent coughing - rhonchi - o2 desat or vital changes - dyspnea - restlessness - increased peak inspiratory pressure or high pressure alarms - |
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suction method
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1-3 passess for 10s or less, pre oxygenate for 30 s before and after and rest between passes
hyperinflation can also be used instead of hyperoxyg. |
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readiness to wean
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- RR<25
- NIF > -20 cm H2O - spont TV 4-5 ml.kg - vital capacity is 10-15 ml/kg - minute ventilations 5-10 L/min - good ABGs without high FiO2 or PEEP (<5) - adequate LOC - good nutrition and hydration - no infection, anemia, fever, etc. - mental readiness - minimal resp depression meds ** know pts baseline of all of this |
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high CO2 vs hypoxia neurologically
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decreased LOC = high Co2
restlessness - hypoxia |
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Cerebral perfusion pressure (CPP) =
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MAP- ICP
normal is 60-100 mm Hg with brain pathology must be maintained > 70 mmHg Any factor that increases ICP and decreases MAP will affect CPP if can't lower ICP, increase MAP to off set it. Sometimes when ICP rises MAP will also. If so, avoid lowering MAP because that will decrease CPP and be BAD :) |
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MAP =
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1/3 PP + DBP
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Causes of ICP
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- Increased circulating blood volume
- increased brain volume - Increase in CSF |
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causes of increased circulating cerebral blood volume
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-- impaired autoregulation, hypercarbia, hypoxia (endotracheal suctioning, airway obstruction)
- metabolic demand (fever, pain, bathing, noxious stimuli, REM, seizure) - impaired venous outflow (increased intrathoracic or intraabdominal pressure) |
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reasons for increased intrathoracic or abdominal pressure
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- abnormal neck positions (want neutral)
- tightly applied trach/endo ties - tumor - valsalva maneuver - PEEP - hip flexion |
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Reasons for increased brain volume
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- cerebral edema (vasogenic- blood brain barrier breakdown so bigger proetins can get in (brain injuries, meningitis, tumors, abscesses) OR cytotoxic- hypoxia or hypoosmolar)
- extra contents (hematoma, tumor, |
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Reason for increase in CSF
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hydrocephalus
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Normal ICP
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0-15 mm Hg (anything over 20 is BAD)
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Normal MAP
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70-90 mmHg
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Normal CPP
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70-90 mmHg (must be greater than 65 to prevent cerebral sichemia)
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S/S of increased ICP
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- HA, nausea/vomiting (may not have nausea before vomiting)
- decline in LOC (know baseline!, may not know if it is a traumatic injury)- rule out stroke, cardiac, sodium problems, etc. - pupillary changes (sluggish to no reaction, increasd saize, papilledema) - motor deficits (focal or abnormal posture) - seizures (new onset at injury due to edema, swelling VS. come later on) - early vital sign changes- hypertension, tachypnea (central neurogenic hyperventilation) - late vital changes- slow, bounding pulse, irregular respirations, increased systolic blood pressure with widening PP (make sure CNAs, etc tell you vitals!) |
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Cushings triad
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LATE sign of increased ICP
- systolic hypertension with widening PP - bradycardia - irregular respirations |
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ICP management (medical)
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- caution not to hyperventilate (keep CO2 35-45)
- PaO2 above 80 (<50 will cause ICP) - Mannitol (watch electrolytes, bp and rebound ICP) - hypertonic saline - loop diuretics - corticosteroids - reduce metabolic demands (barbituate, propofol, prevent fever, seizure control, neuromuscular blockade) - ICP monitoring (for ICP and CPP) - fluid filled (like hemodynamic) and fiberoptic and filament sensors |
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BP management
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- do not lower BP (avoid hypotension)
- keep MAP at 70-90 - watch use of CCB, which can cause vasoconstriction and increased ICP - use labatalol of BP control needed, but HTN may be needed - nicardipine |
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Nursing care of ICP monitoring system
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- compare neuro assessments
- maintain closed system - monitor for infection - change dry steril gauze according to protocol - position system appropriately - callibrate per system requirements - Record ICP and CPP, report changes to physician |
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nursing care of ICP pt
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- assure adequate oxygenation (but not hyperventilated which will cause retaining CO2)
- 40-45 degrees if appropriate (eval BP, increased HOB may decrease MAP and CPP, if CPP stays low reposition, flat if needed) - neck neutral - suction only as needed (10 s, no more than 2 passes, pre oxyg.) - fluid admin - family visitation (avoid excess stimulation) - rest periods between activities - assess response to visitors - ongoing assessment, report changes - avoid fever, seizures, agitation, pain |
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Epidural hematoma
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- between skull and dura mater
- frequently temporal area - develops rapidly "talk and die" - emergent surgery - ARTERIAL blood (middle meningeal) |
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Subdural hematoma
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- below dura mater, may be bilaeral
- VENOUS (cortical vein) - may be associated with contusions, falls - acute, subacute, chronic - requires burr hole surgical drainage |
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S/S of subdural hematoma
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- acute- early signs (HA, irritable, restless, foacl deficit, progressive unconsciousness)
- subacute- presentation usually less severe -chronic- HA and mental status changes, subtle focal deficits |
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Autonomic dysreflexia
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T6 or above after resolution of spinal shock
- intense sympathetic response to stimuli (kinked cath, impaction, skin (tight clothing, irritation from linens) --> HTN, HA, bradycardia, nasal congestions, blurred vision, profuse diaphoresis ABOVE the level of the lesion, flushing of face and neck, pallor, chills, pilomotor erection BELOW level of injury, anxiety --> assess and remove cause |
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S/S of aneurysm
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- sudden "worst HA of life"
- seizures - change in sensorium - nuchal rigidity (meningeal irritation) - focal deficits |
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post aneurysm seizures
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- usually within 12 hours post rupture (du to ICP and re-bleeding)--> don't treat at this point
- after 12 hours secondary to ischemia ( seizure prophylaxis not rec unless seizures occur after 12 hours) |
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Cerebral vasospasm
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- leading cause of death post aneurysm
- narrowing of arteries adj to aneurysm causing ischemia and infarction (lowers CPP) - 3-14 days post rupture - headache (thunderclap HA, rapid, not dull), neck stiff, fever, confusion, hemiplegia |
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CN I
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olfactory, smell
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CN II
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Optic, vision
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CN III
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oculomotor, movement of eyes and constriction
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CN IV
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Trochlear, movement of eyes
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CN V
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Trigeminal, chewing, scalp sensation, face, teeth
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CN VI
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Abducens, movement of eyes
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CN VII
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Facial, facial expression, lacrimation, salivation, taste of anterior tongue
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CN VIII
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Auditory, hearing, equilibrium
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CN IX
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Glossopharyngeal, swallowing, post tongue taste, pharynx
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CN X
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Vagus, swallowing, laryngeal, parasympathetic function
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CN XI
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Spinal accessory, movement of head and shoulders
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CN XII
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hypoglossal, movement of tongue
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Gold standard for inflammatory conditions of the brain
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lumbar puncture
#1!!! |
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Acute renal failure oliguria
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output < 400 mL.day
anuria is less common in acute renal failure |
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Intrarenal factors/causes
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- alterations in nephron function
- diabetic nephropathy - chemical damage to nephron (renal toxic drug) - prolonged hypertension - prolonged pre renal causes - actue tubular necrosis (ischemia, hypotension, hypovolemia, obstetric complications, nephrotoxic agents, radiocontrast, transfusion reaction, rhabdomyolisis, heavy metals) - glomerulonephritis (post strep) - vasculitis - malignant HTN - SLE, DIC, scleroderma - bacterial endocarditis - pregnancy HTN - renal artery thrombosis * if pt has been compromised, put foley in and immediately dump it before starting to measure |
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Nephrotoxic agents
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aminoglycosides
radiographic contrast material |
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predisposing factors to intrarenal ARF
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- advanced age
- diabetes - dehydration |
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Initiation phase
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- event to change in urine output (several to 24 hours after event)
- reduced perfusion but no damage yet |
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Maintenance phase (oliguric phase)
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- acidosis, hyperkalemia, low urine output
- GFR 5-10 ml/min - some nonoliguric - serum creatinine and BUN elevate |
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Recovery phase (diuretic phase)
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renal injury repaired, normal function again, diuresis
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Electrolytes in renal failure
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acidosis
hyponatermia hypocalcemia hyperphosphatemia hyperkalemia |
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Most accurate lab
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creatinine clearance- would be decreased
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BUN/Creatinine ratio
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Normal 10:1 to 20:1
- if ratio grater than 20:1 then cause is other than renal (dehydration, high protein, starvation, GI bleed, steroid, fever) - acute tubular necrosis (intrarenal) has a normal BUN/ Creatinine ratio! |
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Other labs to measure
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urine sediment
urine electrolyte urine cells, casts, and crystals blood creatinine (not as good as clearance) - daily weights (1kg = 1L of fluid) urine specific gravity- but not as useful |
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Normal urine output
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0.5-1ml.kg/hr
oliguria is < 400mL in 24 hours |
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Nursing intervention sin ARF
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- I&O
- daily weights - infection prevention/asepsis (high risk!) - peak and trough for drugs (gentamycin, etc.)- peak is 1-2 hours after admin of drug, trough is before admin |
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Management of ATN
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- prevention = early identification!
--patient factors and treatment factors --maintian hydration (perioperatively, invasive procedures, dx contrast dyes) --maintain renal perfusion (vasoactive drugs) --careful drug monitoring and drug/drug interaction assessment |
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Pharmacological management of ARF
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diuretics (contraversial)
- may increase risk if given before procedures - may only increase urine flow and not GFR Dopamine- contraversial (less than 5mcg/kg/min) - may cause tachydysrhythmias Mucomyst (acetylcysteine) - prophylactic 600mg BID of day of procedure with hydration Epogen (anemia) adjust established regimens |
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Dietary management
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- high energy needs
- lose protein and vitamins in dialysis - fluid restriction (output plus 600-1000ml.day) explain to family - multivitamin, folic acid - sodium restriction (fluid overload) - manage hyperkalmia (dialysis, calcium gluconate, glucose/insulin, K restriction) |
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Renal replacement therapy
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hemodialysis- in critically ill pts may have temporary dialysis cath (vascular) put in
continuous renal replacement therapy (may be preferred in pts that are hemodynamically unstable) - a gradual 24 hour process peritoneal dialysis |
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sodium allowed
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0.5-1 gram/day
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hyperkalemia on ECG
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6-7 = peaked T waves
7-8 = peaked T waves, flat P, prolonged PRI, depressed ST segment 8-9= peaked T waves, prolonged QRS, atrial standstill >9= sine wave pattern (looks like 2 peaked T waves depression between and before and that's it) |
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highest morbidity for burns
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- burns over more than 50% of BSA
- older pt - younger pt |
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Elderly risks- SKIN
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- less resilient to mechanical trauma
- loss of atrophy of hermal and subcu mass - reduced microcirculation - manifest a skin thinning and predispose for deeper burn wounds and poor or delayed healing |
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Elderly risks- IMMUNE
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healing impacted be lowered immune system and susceptible to infection
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Elderly risks- RESERVE
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- low physiologic reserve and capacity to respond to significant metabolic stress, hemodynamic demand, and inflammatory challenge that occur after a burn injury
- preexisting conditions make it worse in shock fluid resuscitation and increase morbidity and mortality |
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Edema in burns
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- burned and unburned areas
- fluid resuscitation (volume and oncotic pressure affects) as well as increased capillary permability increase edema - max edema is 18-24 hours after burn - occurs in burn areas and also distant systemic unburned tissue and organs - further exacerbated by decrease in lymph drainage - edema is usually a normal response, but in burns it exceeds the intended beneficial inflammatory effect - continues to expand till it reaches a max at 24 hours -reabsorption occurs 1-2 days after burn injury - in burns greater than 20% leads to burn shock--> decreased CO |
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Methods of injury in chemical burns
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- contact
- inhalation of fumes - ingestion or injection |
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Management of chemical injury
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- systemic and local effects
- must be completely removed or neutralized or damage continues - use MSDS - systemic effects: cns depression, hypothermia, hypoTN, pulmonary edema, intravascualr hemosysis - watch for inhalation bronchitis and pneumonitis - hepatic and renal problems - alkali-cleaning products - acids- bathroom cleaners, rust removers - organic compounds- phenols, petroleum (gas) |
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AC vs. DC
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AC (alternating contact) has higher cardiac arrest (vfib) and tetanic muscle contraction
DC (direct contact) -lightning, car batteries lightning has high cardiac arrest (like 70%) |
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Electrical injury
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- electricity converts to heat, greatest damage is a point of contact (entry and exit)- usually extremities
COMPLICATIONS: - renal (muscle damage) -cardiac arrest |
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Inhalation injury
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carbon monoxide
- can be above or below the glottis |
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S/S of upper airway/above glottis
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edema and risk for airway obstruction
- hoarseness - dry cough - labored or rapid breathing - difficulty swallowing - stridor |
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lower airway injury/below glottis
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- carbonaceous sputum (soot in secretions) **hallmark sign**
- tracheal and bronchial constriction and spams with wheezing can occur within minutes to several hours--> ARF and ARDS within a few days - impaired ciliary activity - erythema - hypersecretion - edema - ulceration - increased blood flow - bronchi or bronchiole spasms - mucosal sloughing within 4-5 days |
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Full thickness burns (3rd degree)
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- destruction of all layers down past fat, fascia, muscle, or bone
- thick, dry leathery appearance (eschar) - no pain - always required skin grafting wound closure |
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Local response to burns
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acute inflammation --> release of mediators that cause vasoactive, cellular, and cardiovascular effects
- altered vascular permeability - burned and unburned areas have increased capillary permiability - vessel walls become porous and leaky - third spacing (fluids, electrolytes, all) - direct thermal damage to blood vessels--> intravascular coag and no blood to wound - max edema 24-48 hours after |
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Burn chock
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combo of distributive and hypovolemic
** fluid resus important in burn management! |
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Cardiovascular and pulmonary response to burns
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- hypovolemia
- decreased CO - tachycardia and vasoconstriction - pulmonary HTN - direct injury |
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renal response to burns
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- sens to decreased CO
- initial decrease in UOP related to decreased GFR - followed bu diuresis (48 to 72 hours) as fluids shift (hourly UOP is optimal measurement of fluid status during immediate fluid resuscitation) |
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prehospital care
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extricate to safety
stop burning process (NEVER apply ice, it furthers burning process!) - remoe jewlelry (metal), remove saturated clothing and cool down, adherent clothing is not removed - remove source of electrical injuries 100% oxygen--> pulse ox may not be accurate identify life threatening injuries minimize time on the scene water lavage of chemical injuries, NO neutralizing agents (causes heat production) possible c spine and intubation protect yourself from injury (gloves, gowns, goggles, face shield) |
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when pt intubated
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* airway obstruction/STRIDOR needs intubation
- severe facial burns are prophylactically intubated because delay may make intubation difficult |
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hourly vitals
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HR, cardiac rhythm, BP, respirations, temp, peropheral pulses
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what to check q 2 hrs
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urine specific gravity, urine glucose, ketones, occult blood tests, gastric pH
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decreased BP
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LATE sign of hypovolemia (because of compensatory mechanisms), but pt may be tachycardic before and cuff readings may be altered by other factors
may be increased from pain, fear, or anxiety also |
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If pt is alert (as severely injured burn pts usually are) then changes
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- look for head injury, CO poisoning, or drug OD
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when NG inserted
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when burn >20% to prevent aspiration
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Types of fluids- LR
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LR (crystalloid)
- no dextrose which is good - contains lactate to buffer metabolic acidosis - does not have intravascular protein replacement (to increase oncotic pressure) - need large amount |
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Fluid resuscitation
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- based on %TBSA (9's, pts pal, lund browder)
- greater than 20% TBSA burns get fluid resuscitation Adults - 2-4ml/kg per % (2-4ml x kg x %) TBSA burned - admin half of total fluids within first 8 hours from time of injury - administer other half over the next 16 hours from time of injury - maintain UOP of 30-50ml/hour - place IC access (2) in nonburned areas - hold colloids (albumin) for 8-12 hours after injury (when cap permeability is highest and will reduce edema and burn shock) potassium may also be added for K lost in urine |
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Fluid resuscitation in electrical injuries
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* Pt's need higher volumes
- keep UOP at 75-100 ml/hr - to prevent renal damage from myoglobinuria (rhabdomyolysis) |
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Labs to monitor for burn pts
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- Na, K (high shows tissue damage and need for cardiac monitor)
- BUN - serum lactate (should be low if fluid resuscitation is good) - carboxyhemoglobin (CO poisoning and is drawn if smoke inhalation is suspected) - chest xray - temp: PREVENT HYPOTHERMIA |
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management of burns on extremities
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- need adequate circulation and want to maintain function
- elevate hands above heart on slings - fingers/toes wrapped individually to prevent webbing - PT/OT, ROM |
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Pain management of burn pt basic
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- acute phase of recovery has resting or constant pain
- and shorter peaks of pain for procedures, dressing changes, therapies, etc. |
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Pain control
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- adequate, frequent assessment tools (before, during, and after procedures)
Opiates--> morphine is drug of choice - IV route (subcu and MI are ineffective because of impaired circulation and edema) -PCA may be useful Anxiolytics nonpharmacological strategies - relaxation, guided imagery, make sure to explain care plans, etc to reduce anxiety |
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ONLY Permanent graft
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autograft- full thickness always needs
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pulse monitoring
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especially important for distal circulation in burns of extremities
can use doppler if compromise, may need escharotomy |
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Nutrition with burn pt
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* important in pt survival
- stressed induced hypermetabolic catabolic state (at risk for neg nitrogen balance due to high caloric need from increased metabolism) |
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2nd 24 hours of burn fluid resuscitation
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Parkland formula
- dextrose in water plus potassium to maintain normal electrolyte balance - colloid-containing fluid at 2-60% of calculated plasma volume which equals an infusion rate of approx: 0.35-0.5 ml/kg/%TBSA |
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assessment of fluid resusc.
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- UOP 30-50 or electrical 75-100 ml/hr
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3rd degree/full thickness care
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- grafting
- prevention of infection - improve and maintain function - splints, ROM - promote would care plan and involve entire team to promote compliance - proper documentation to promote compliance - wound care and prevention of infection |
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S/S of hypoxemia
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- anxiety
- restlessness - confusion - fatigue - combative/agitation - coma |
