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283 Cards in this Set
- Front
- Back
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normal range of pH
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7.35-7.45
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normal range of pCO2
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35-45mm Hg
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normal range of HCO3
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22-26 mEq/L
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respiratory component of ABG
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pCO2
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metabolic component of ABG
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HCO3
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how do you determine full or partial compensation in an ABG
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if pH is normal, full compensation; if opp component is normal NO compensation
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when assessing the airway what precautions are important to maintain with trauma patients
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C-spine
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#1 cause of an obstructed airway in conscious pt
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food
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#1 cause of an obstructed airway in unconscioius pt
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tongue
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what object can we use to align the airway properly
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small towel beneath shoulders
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when do we use jaw thrust
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when trauma is suspected
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when is an oropharyngeal airway appropriate
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used to maintain airway of unresponsive pt who has no gag reflex
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how do we determine appropriate size for an OPA
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corner of the mouth to the tip of the earlobe
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when do we use a nasopharyngeal airway
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in patients that still have an intact gag reflex
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how do we measure for a nasopharyngeal airway
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from the tip of the earlobe to the tip of the nose; should also fit in diameter of nose
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the beveled edge of a nasopharyngeal airway goes where
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against the septum
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what is the purpose of RSI
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to facilitate endotracheal intubation with the least likelihood of aspiration
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what can you ask the pt to do to tell if they are able to protect their airway
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swallow(best) or cough
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what MUST we do prior to RSI
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preoxygenation (over 5 mins if possible)
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after preoxygenation and before intubating what do we need to give to pt
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LOAD (lidocaine, opiate, atropine, defasciculation) for comfort
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sellick's maneuver
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pressure on the cricoid cartilage to prevent passive regurgitation of gastric contents
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when intubating, the tube goes where
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in between vocal chords
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techniques used for confirmation of placement of ET tube
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end tidal CO2(gold standard), misting, pulse ox, breath sounds, colormetric end tidal CO2, aspiration techniques
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which vital sign usually indicates inadequate sedation after intubation
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hypertension
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class I airway
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fully visible uvula; open space in back of mouth
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class II airway
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uvula still visible; tongue partially covers open space
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class III airway
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no open space; uvula only partially visible
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class IV airway
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no open space; uvula not visible
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what do we do if SaO2 goes down after intubation
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DOPE; dislodged, obstructed, pneumothorax, equipment failure
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when is an adjunct airway indicated
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failed airway not due to foreign body obstruction; skill level does not permit intubation; ET felt to be impossible
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when is an adjunct airway contraindicated
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pt is responsive; intact gag reflex; known esophageal disease; ingestion of caustic substances; upper airway obstruction due to foreign body
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describe a laryngeal mask airway
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designed to cover supraglottic area; used as temporizing agent in failed airway; pt must be sedated
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indications for chest tubes
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remove air, fluid, remove blood, restore negative pressure, re expand collapsed lung, pleural or mediastinal after surgery, drainage holes, radioopaque marker
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chest tube location
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for air: 2nd or 3rd ICS MCL, directed toward apex; for fluid: 5th or 6th ICS, MAL, directed posterior
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after inserting chest tube what do we need to do?
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CXR to r/o pneumothorax/trauma and confirm location
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what is a heimlich flutter valve
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treatment of pneumothoraces; one way valve allows air to escape but not re-enter pleural space
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how is the water seal chamber used
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fill to 2cm sterile water
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what does bubbling in the water seal chamber indicate
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air leak
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describe tidaling as related to a chest tube
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fluctuation in water seal chambers fluid level that corresponds with respiration
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the water in the water seal chamber goes which direction upon inspiration/expiration
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inspiration-rises; expiration-falls
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in a mechanically ventilated pt how does the water in the water seal chamber move
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inspiration-fall; expiration-rise
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if the water seal chamber has no movment what may be indicated
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occluded chest tube or lungs are fully expanded
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when is it appropriate to clamp a chest tube
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assessing for air leak; prior to removing CT; sclerosing
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when should we NOT clamp a chest tube
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if there is an air leak from the lung-will cause a pneumothorax; during transport
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how do we determine where the air leak in a chest tube is
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indicated by continuous bubbling; clamp CT close to dressing; if bubbling stops leak is at site of insertion or within chest; if continues, between clamp and drainage system
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list some appropriate nursing interventions for CT
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semi fowlers or elevate HOB; keep all tubes straight; keep drainage system below chest level; all connections taped; do not strip or milk tubing
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a sudden increase in CT drainage indicates
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hemorrhage or sudden patency of previously obstructed tube
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a sudden decrease in CT drainage indicates
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CT obstruction or failure of CT or drainage system
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what do we do if CT falls out or accidentally pulled out
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quickly seal off site; use petroleum guaze covered with dry gauze and occlusive tape to prevent air from re-entering cavity
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what is SIRS
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systemic inflammatory response syndrome; systemic level of acute inflammation, that may or may not be due to infection
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s/s of SIRS
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fever, hypothermia, tachycardia, tachypnea, elevated WBC, impaired gas exchange, metabolic acidosis, oliguria, hyperbilirubinemia, coagulopathy
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labs affected by DIC
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decreased platelet count, prolonged FDP, decreased factor assay, prolonged PT, prolonged APTT, prolonged thrombin time, decreased fibrinogen, prolonged D dimer, decreased antithrombin
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indication for platelet factor 4 antibody test
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to identify antibodies to platelet factor 4 leading to heparin induced thrombocytopenia and excessive bleeding
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why are cortisol levels important
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may show problems with adrenals or pituitary
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why are lactate levels important
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indirect assessment of oxygen levels in blood; may determine course and cause of lactic acidosis
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one of the most important and early interventions in tx of sepsis
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rapidly identifying source/fluids?
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what does an increase in eosinophils indicate
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parasitic infestation, collagen vascular disease, addisons, allergic reaction
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normal resp rate on ventilator
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8-12 breaths/min
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normal tidal volume on vent
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5-8 ml/kg ideal body weight
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normal tidal volume
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10-15 ml/kg ideal body weight
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why is the tidal volume on mech vent lower
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positive pressure can create damage to lungs if we overfill
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minute volume
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volume of air that is moved through the lungs over 1 minute
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normal minute volume
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5-10 L
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which resp measurement is a good indicator of diaphragm function
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vital capacity
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vital capacity
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maximum amount of air exhaled after a maximum inspiration
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normal vital capacity
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65 ml/kg ideal body weight
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FiO2
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fraction of inspired oxygen; amount of oxygen being delivered
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when does oxygen toxicity occur in relation to FiO2
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FiO2 > 50-60% for > 24 hours
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what is the lowest level of PaO2 we can accept and still adequately load hemoglobin
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60%
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purpose of lidocaine before intubation
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increases depth of anesthesia, suppresses cough reflex
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purpose of fentanyl before intubation
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suppresses resp effort; opiod analgesic
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adverse effects of fentanyl
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hypotension
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etomidate use
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sedative/induction agent
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adverse effects of etomidate
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involuntary myoclonic movements; adrenal suppression
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midazolam uses
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anxiolytic, induction of anesthesia, sedation, anticonvulsant, amnestic
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indication for propofol
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induction of anesthesia
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adverse effect of propofol
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significant hypotension
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2 classifications of muscle relaxants
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depolarizing neuromuscular blocking and non depolarizing
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classification of succinylcholine
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depolarizing NMBA
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contraindications for succinylcholine
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hyperkalemia; hx of malignant hyperthermia; ongoing neuromuscular disease
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why do we not redose succinylcholine
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cases of profound, unrecoverable bradycardia
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non depolarizing NMBAs can be reversed by what
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acetylcholinesterase inhibitors
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examples of non depolarizing NMBA
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mivacron, vecuronium, rocuronium, pavulon
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what are the 4 factors of respiratory function
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neurochemical control of ventilation; mechanics of breathing; gas transport; control of pulmonary circulation
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which respiratory center is responsible for normal rhythmic breathing
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dorsal respiratory group
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define negative inspiratory force or negative inspiratory pressure
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how much negative pressure change can the pt generate with max inspiratory efford
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normal range of NIF/NIP
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neg 80 to -100 cm H2O
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describe peak inspiratory pressure
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how much pressure is reached in the lung at the peak of inspiration
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at what PIP does does volutrauma occur
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50+ pressures
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when the patient's PIP does not match the set PIP what should we do
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listen to lungs; can indicate fluid overload or secretion buildup
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describe PEEP
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positive end expiratory pressure; pressure that is maintained in the lungs at the end of expiration
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what is the normal level of PEEP normally maintained in our lungs
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5cm
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what does PEEP do for our lungs
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keeps the alveoli open at the end of exhalation; diseased lungs can have no PEEP
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at what level does PEEP get too high
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>15
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what are the effects of high PIP and PEEP
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increased volutrauma, increased chance for pneumothorax, decreased venous return to heart, may cause hypotension, increase auto PEEP
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what does the sensitivity setting on a ventilator do
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controls the amount of pt effort needed to initiate an inspiration; measured by NIF
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normal setting for sensitivity
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neg 2
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list some indications for mechanical ventilation
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supporting gas exchange, lung volume, work of breathing, reverse hypoxemia and resp acidosis, relieve resp distress, stabilize chest wall, decrease O2 consumption
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types of ventilators
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negative pressure-applied externally to pt; positive pressure-forces air into lungs via ET tube or trach-used today
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three parameters that control mechanical ventilation
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trigger, limit, cycle
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mech vent trigger
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event that begins inspiration; can be pt initiated or machine initiated
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mandatory breath
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vent delivers breath by itself
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spontaneous breath
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initiated by pt
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mech vent limit
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limits set to maintain airflow during inspiration; flow rate (IFR), set pressure(PIP), volume limited (VT)
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mech vent cycle
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event that ends inspiration; volume cycled, pressure cycled or pressure support
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modes of mech ventilation
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assist control; synchronized intermittent mandatory ventilation (SIMV); pressure support (PSV); continuous positive airway pressure (CPAP); bilevel positive airway pressure (BiPAP)
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initial mech vent mode of choice
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assist control (AC)
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describe basics of assist control
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set Vt, RR, FiO2 &/or PEEP; trigger is either machine or pt; if pt, machine still delivers set amounts
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describe SIMV
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Vt, RR, FiO2, PEEP and sensitivity are preset; trigger may be spontaneous or mandatory; on pt initiated breaths, machine does not deliver any volume
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describe PSV
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no set Vt or RR; pt's effort determines RR, IFR, Vt; delivers air to set pressure early in inspiration
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which vent mode is used for weaning and extubation
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PSV
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which two modes can be used in conjuction
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SIMV and PSV
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describe CPAP
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positive pressure maintained through resp cycle; similar to PEEP
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what is CPAP used for
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weaning mode; nocturnal ventilation; OSA
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describe BiPAP
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provides both inspiratory and expiratory pressure support; pressures can be different
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what is BiPAP used for
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weaning; hypoventilation; sleep apnea
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a low pressure alarm on vent usually indicates
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cuff leak; dislodged ET tube; broken circuit
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PIP alarm can indicate
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decreased compliance; kinked ET tube; mucous plug; increased secretions; water in circuit; pneumothorax
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when vent is not working correctly what do we do first
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DOPE; dislodged, obstructed, pneumothorax, equipment failure
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why do we warm and humidify air from artificial airways
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no humidification leads to mucous plugs, secretions, drying out of airway
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a pt on a vent should always also have what
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some kind of gastric decompression
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positioning for pt on vent
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HOB up 30 degrees
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how do we prevent ARDS and VAP
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handwashing and frequent oral care
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volutrauma
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barotrauma; mech vent and PEEP can over distend and rupture alveoli air leaking
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how can a vent cause cardiac complications
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increased intrathoracic pressure causes decreased venous return to heart=decreased preload=decreased CO=decreased hepatic, renal, CNS perfusion
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how often do we change ETT tape/ties
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every 24 hours; move to other side of mouth
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when adjusting ETT, what do we always do
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auscultate breath sounds after repositioning, changing tube or ties
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before weaning from vent, what must be addressed
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reason for resp distress must be fixed or weaning will fail
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sepsis
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inflammatory process that is out of control
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MODS
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multiple organ dysfunction syndrome; begins with sepsis
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primary cause of MODS
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cell death related to severe ischemia or sepsis
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what system is usually first to fail with MODS
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respiratory
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4 phases of MODS
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general increased capillary permeability, hypermetabolic state, organ malfunction, organs return to normal and/or permanent damage (death)
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major treatments for shock and MODS
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adequate fluid resuscitation; support cardiac function; support ventilation; adequate nutrional support; sedation
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which blood gas crosses the brain barrier and what happens when it does
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CO2; when hydrogen ions are detected resp rate and depth increase
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compliance
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measure of distensibility; determined by alveolar surface tension and elastic recoil
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which resp disorder has too much compliance? Too little?
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COPD too much; pneumonia too little
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2 primary components of ventilation
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resp rate and tidal volume
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best indicator of diaphragm function
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vital capacity
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what does seesaw breathing indicate
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indicates diaphragm is not functioning
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hypoxia vs hypoxemia
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hypoxia=lack of available oxygen; hypoxemia=problem with oxygen transport
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what does clubbing of the fingers indicate
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chronic hypoxic conditions
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the trachea deviates to what side with tension pneumothorax
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away from affected side
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the trachea deviates to what side with severe atelectasis
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towards affected side
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how do we assess neck vein distention
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HOB elevated; collapse upon inspiration; distend on expiration
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why do distended neck veins collapse upon inspiration
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thoracic pressure increases
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kussmaul's respirations
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fast and deep; assoc with DKA
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cheyne stokes respirations
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alt periods of deep and shallow with apnea; head injuries
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biot or ataxic respirations
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no pattern; irregular with apnea; severe head injuries; generally from ICP pushing on brain stem
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what causes subcutaneous emphysema
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large leaks in airway; ventilator pressure; chest tube not patent; CT drainage port beneath skin and not in pleural space
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bowel sounds in chest indicate
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ruptured diaphragm
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egophony
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ee sounds like ay; indicates consolidation
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bronchophony
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99 sounds very loud and clear; indicates consolidation
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whispered pectoriloquy
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can hear whispered sounds upon auscultation; should not be able to; indicates consolidation
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normal PaO2
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80-100
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why does the apex of the lung have less circulation
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alveolar pressure is greater than blood pressure
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type 1 alveolar cells
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provide structure and fluid barrier
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type 2 alveolar cells
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produce surfactant
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type 3 alveolar cells
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macrophages
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what is surfactant and what is its function
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lipoprotein that facilitates expansion during inspiration
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V/Q balance
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ventilation=perfusion
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a low v/q balance indicates
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bad ventilation, good perfusion; ex: asthma
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a high v/q balance indicates
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lots of volume, bad perfusion; ex: COPD
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low v/q ratios caused by
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pneumonia, atelectasis, tumors, mucous plug
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high v/q rations caused by
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PE, pulmonary infarct, cardiogenic shock, mech vent
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silent unit
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both v/q are decreased; ex: pneumothorax, severe ARDS
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normal PaO2/FiO2 ratio
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>400
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What ratio of PaO2/FiO2 indicates ARDS
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<200
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acute respiratory failure
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when the pulmonary system fails to maintain adequate gas exchange
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hallmark symptom of ARF
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hypoxemia or hypercapnia
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hypoxemic ARF caused by
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disorders that interfere with O2 transfer to blood; pneumonia, PE, pulmonary edema, alveolar injury secondary to inhaled gases; alveolar damage second to ventilation; decreased CO, heart failure
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hypercapnic ARF caused by
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insufficient CO2 removal; increased CO2 with decreased pH; drug OD, CNS depressant, neuromuscular diseases, trauma to CNS, acute asthma
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pulmonary embolism
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obstruction of pulmonary artery or its branches by a thrombus/emboli that originates in the venous system or right heart
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hallmark of ARDS
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pulmonary edema in the absence of cardiac failure
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three phases of ARDS
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exudative, proliferative, fibrotic
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s/s of exudative phase of ARDS
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restlessness, apprehension, progressive dyspnea and tachypnea, moderate use of accessory muscles, breath sounds usually clear, mild resp alkalosis
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s/s of proliferative phase of ARDS
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agitation, increased resp distress and excessive accessory muscle use, fatigue, fine crackles, refractory hypoxemia, hypercapnia, resp acidosis, CXR whiteout
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pulmonary contusion
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assoc with chest trauma; rapid compression and decompression of chest wall
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manifestations of pulmonary contusion
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interstitial and intra-alveolar hemorrhage; alveolar edema; atelectasis
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flail chest
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free floating rib segments; ribs suck in when breathing; can lead to lung punctures
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criteria for referral to burn unit
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2nd & 3rd degree over 10% TBSA; all 3rd degree over 5%; suspecting inhalation; electrical; chemical; pedi; burn victims with coexisting diseases; burns of hands, face, feet, genitalia, major joint
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describe the rule of palms
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used for scattered burns; the patient's palm size is 1% of their body
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what #s correspond to what body part with rule of 9s
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9 for chest, back, abdomen, lower back, front of legs, back of legs; 4.5 for face, back of head, front of arms, back of arms; 1 for genitalia
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what causes tissue to continue to be destroyed for 48 hours post burn injury
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release of local mediators; immune inflammatory response; coagulation system
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3 zones of injury
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zone of coagulation, zone of stasis, zone of hyperemia
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describe first degree burns
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heal w/o intervention, superficial, epidermal layer only, pink to red w/ no blisters
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describe second degree burns
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partial thickness, epidermal and dermal layer involved, red mottled pink edges, hair intact, blanches to touch, 1-6 weeks to heal
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describe third degree burns
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full dermal layer involved; white, chery red, charred, leather like texture; no clear pain, insensate, may ache
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inhalation injuries can be caused by
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carbon monoxide, soot, chemical, thermal, aspiration
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hallmark sign of CO poisoning
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cherry red cheeks
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baxter/parkland formula
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fluid resuscitation; weight in kg X TBSA X 4ml
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what fluid do we use for burn pt replacement
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lactated ringers
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at what rate do we admin the amount figured with baxter/parkland formula
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1/2 in first 8 hours; other half in following 16 hours
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three major phases of burn management
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resuscitative, reparative, rehabilitative and reconstructive
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first thing we address with burn victims
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ABC!
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what do we address in the resuscitative phase of burn care
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protect the team, ABCs, protect airway, fluid needs, metabolic and electrolyte, psychosocial
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what needs are addressed in the reparative phase of burn care
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wound care; nutritional support; management of pain; prevention of contractures; wound management; psychosocial
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needs addressed in the rehabilitation and reconstruction phase of burn care
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on going skin needs; activity needs; self concept and depression; noncompliance with care
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pathophysiology of a burn
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burn-vascular permeability-edema-decreased blood volume-increased peripheral resistance-burn shock; decreased intravascular volume-increased hematocrit-increased viscosity-increased peripheral resistance-burn shock
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3 things that usually cause cord compression
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bone displacement; interruption of blood supply to cord; traction resulting from pulling on cord
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2 types of spinal cord injury
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cord compression, penetrating trauma
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primary spinal cord injury
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initial mechanical disruption of axons as a result of stretch or laceration
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secondary spinal cord injury
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ongoing, progressive damage that occurs after initial injury
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what secondary injuries cause the most damage to the spinal cord
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edema secondary to inflammatory response; causes ischemic damage
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describe spinal shock
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temporary neurologic syndrome; characterized by loss of reflexes, loss of sensation, flaccid paralysis below level of injury; experienced by 50% of acute spinal cord injuries
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describe neurogenic shock
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loss of vasomotor tone caused by injury; characterized by hypotension and bradycardia; peripheral vasodilation, venous pooling, decreased cardiac output
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major mechanisms of spinal injury
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flexion or hyperflexion; hyperextension; compression or axial loading; rotational
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how does hyperflexion injury the spinal cord
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compression, dislocation, instability, ruptured ligaments
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how does hyperextension injure the spinal cord
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head accelerated and decelerated; vertebrae may fracture or subluxate; spinal cord stretched and distorted; contusion and ischemia of SC
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describe axial loading
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vertical force along SC (landing on feet, butt, head); vertebrae shatter (wedge, burst or teardrop fx); bone fragments damage SC
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how does a rotational injury damage the SC
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tearing of posterior ligaments; displacement of the spinal column
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central cord syndrome
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occurs most commonly in cervical area; motor weakness and sensory loss are present in both upper and lower extremities; greater loss in arms than legs
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anterior cord syndrome
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compromised blood flow to anterior spinal cord
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brown sequard syndrome
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damage to one half of spinal cord; loss of motor function and position and vibration sense on same side of injury; paralysis on same side as lesion; opp side has loss of pain and temp sensation below level of lesion
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posterior cord syndrome
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compression or damage to posterior spinal artery; RARE; pain, temp sensation and motor function below level of lesion remain intact
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immediate post spinal cord injury problems
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patent airway; adequate ventilation; adequate circulating blood volume; preventing secondary damage
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what major resp function is lost with a C3 and above injury
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phrenic nerve function; cannot cough or clear airway
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what major resp function is lost C3-C5 injury
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diaphragmatic innervation; hard to cough or clear airway
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what major resp function is lost with C6-T8 injury
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intercostals
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poikilothermism
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adjustment of body temp to room temp
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issues with temp control below level of spinal cord injury
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below level of injury no vasoconstriction, piloerection or heat loss through perspiration
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criteria for early surgery on spinal injury
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evidence of cord compression; progressive neurologic deficit; compound fx; bony fragments; penetrating wounds of spinal cord or surrounding structures
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what is kinetic therapy
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uses a continual side to side rotation; decreases pressure ulcers and cardiopulmonary complications
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why can return of reflexes complicate rehab
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they can be hyperactive, exaggerated or spastic; family may see this as return of function
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oral meds commonly used for spasticity related to spinal cord injuries
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baclofen, dantrolene, gabapentin
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autonomic dysreflexia
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massive uncompensated cardiovascular reaction mediated by sympathetic nervous system; occurs in response to visceral stimulation; life threatening
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what is the most common precipitating factor for autonomic dysreflexia
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distended bladder or rectum
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s/s of autonomic dysreflexia
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hypertension, blurred vision, throbbing headache, marked diaphoresis above lesion level
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where is an epidural hematoma located
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between dura and skull
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where is a subdural hematoma located
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between outer arachnoid membrane and dura
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where is a subarachnoid hematoma located
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between outer arachnoid membrane and pia mater
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types of noxious stimuli
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nailbed pressure, sternal rub, supraorbital pressure, trapezius squeeze
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describe decorticate posturing
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feet and hands are rotated in
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describe decerebrate posturing
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feet and hands are rotated out
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cranial nerve 1 controls
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olfactory; sensory nerve
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cranial nerve II controls
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optic; sensory nerve; vision, pupil reactivity to light and accomodation
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cranial nerve III controls
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oculomotor; motor nerve; eyelid elevation; most EOMs; pupil size and reactivity
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factors that influence ICP
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arterial pressure, venous pressure, intraabdominal and intrathoracic pressure, posture, temp, blood gases
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normal ICP consists of what 3 components
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brain tissue, blood and CSF
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what ICP component is the first to change under pressure
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CSF; either absorbs or stops producing
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what is CPP
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cerebral perfusion pressure; pressure needed to ensure blood flow to the brain
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how do we figure CPP
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MAP-ICP
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normal CPP
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70-100 mm Hg
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three types of cerebral edema
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vasogenic, cytotoxic, interstitial
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vasogenic cerebral edema
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most common; occurs mainly in white matter; assoc with changes in endothelial lining of cerebral capillaries
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cytotoxic cerebral edema
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mainly in gray matter; disruption of functional integrity of cell membranes
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interstitial cerebral edema
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pt with uncontrolled hydrocephalus
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s/s of increased ICP
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restlessness, increasing drowsiness, pupillary changes, impaired ocular movments, tinnitus, HA, vomiting; change in LOC; cushings triad; decrease in motor function
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two major complications of uncontrolled increased ICP
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inadequate cerebral perfusion; cerebral herniation
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types of cerebral herniation
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tentorial, uncal, cingulate
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when is a pt fitted with an ICP measurement device
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GCS of 8 orless; abnormal CT scan or MRI; hx of neurological insult
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gold standard for ICP monitoring
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ventriculostomy
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inaccurate ICP measurements can be caused by
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CSF leaks; obstruction in catheter; differences in height of bolt/transducer; kinks in tubing; incorrect height of patient's drainage system relative to pt's reference point
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what is the parenchyma in the skull
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brain tissue; wrapped in the pia mater; divided into cerebrum, cerebellum, brainstem
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describe the cerebrum
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cerebral hemispheres are connected by corpus callosum; right and left lobes: frontal, temporal, parietal, occipital; diencephalon
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what does the cerebellum control
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coordination, muscle tone, fine motor activity
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with a head injury, death occurs at which 3 points in time and why
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immediately after injury; within 2 hours due to hemorrhage or edema; 3 weeks later (usually MODS)
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describe the types of skull fractures
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linear-low impact; depressed-severe blow; simple; comminuted-splintered; compound-crossed over
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signs of a basilar skull fracture
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battles sign; conjugate gaze; facial paralysis; spinal fluids from ear or nose
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describe a diffuse axonal injury
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widespread axonal damage occurring after a mild, moderate or severe TBI; not a lucid period of time with this injury; process takes about 12-24 hours
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where does damage occur with a diffuse axonal injury
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axons in subcortical white matter of cerebral hemispheres; basal ganglia; thalamus; brainstem
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clinical signs of a DAI
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decreased LOC, increased ICP, decerebration or decortication, global cerebral edema
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origin of epidural hematoma
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arterial, most often the middle meningeal
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classic signs of epidural hematoma
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initial period of unconsiousness; brief lucid interval followed by decrease in LOC; HA, N/V, focal findings
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most common source of subdural hematoma
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small bridging veins
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signs of acute subdural hematoma
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within 48 hours of injury; drowsy, confused, ipsilateral pupil dilates and becomes fixed; similar s/s as increased ICP
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most common causes of subarachnoid hematoma
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subarachnoid aneurysm, head trauma, hypertension
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s/s of subaracnoid hematoma
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thunderclap HA, nuchal rigidity, photophobia
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how do we treat a berry aneurysm
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Triple H therapy; hypervolemia, arterial hypertension, hemodilution
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what is the lowest possble GCS score
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3
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when do we intubate based on GCS
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score of 8 or less
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what does an abnormal dolls eye movement indicate
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brainstem injury
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describe normal dolls eye
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eyes move opposite direction of head rotation
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describe abnormal dolls eye
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eyes follow direction of head rotation
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what two other signs generally accompany an abnormal dolls eye
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possible loss of gag and cough reflex
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describe the oculovestibular reflex
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cold water in ear; normal-nystagmus, eyes move slowly toward ear and rapid movement away; abnormal-eyes remain fixed at midline position
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what can an abnormal oculovestibular reflex indicate
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severe brainstem damage
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what drugs can cause an inhibition of the oculovestibular reflex
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neuromuscular blockers; barbituates
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criteria for a persisitent vegetative state
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absense of awareness of self; inability to interact with others; lack of language comprehension; brain stem function to maintain life; condition has continued for at least 1 month
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brain death
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irreversible loss of function of the brain including brain stem; repeat eval done at least 6 hours later
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criteria to measure brain death
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absence of corneal reflex and gag reflex; presence of apnea; angiography demonstrates empty head syndrome
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empty head syndrome
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dye does not move through blood vessels in brain like it should
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texas criteria for dr to designate brain death
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intubated and on ventilator; no sedation; GCS less than 5; no response to painful stimuli
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