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39 Cards in this Set

  • Front
  • Back
hypercapneic
metabolic rate > alveolar ventilation
CO2 production > CO2 excretion

ABG definition: respiratory acidosis
- increase PaCO2 (>50) with decrease pH (<7.30)
hypoxemic
inadequate oxygenation
- decrease PaO2 (<60) with O2 sat < 90%
most common type of respiratory failure?
high work of breathing
poor respiratory drive
brain stem suppression
- drugs: narcotics & benzodiazepines
- endocrine/metabolic (hypothyroid)

brainstem damage
- trauma (damage pace maker) intracranial P increase stimulates hyperventilation, so this is rare
- disease (ALS & polio)
poor muscle strength
muscular disorders
neurologic disorders
drugs
muscular disorders in acute resp failure
malnutrition
electrolytes abnormalities
dystrophies, myositities
neurologic disorders that produce poor muscle strength
ALS, polio, MS
spinal cord injury
myasthenia gravis
drugs that produce poor muscle strength
neurmuscular relaxing agents (surgery)
steroids (common)
high work of breathing components
flow/resistive work

stretch work

volume work
flow/resistive work
upper airway obstruction
- aspriation
- produces stridor

lower airway obstruction
- wheezing
stretch work
lung parenchymal stiffness (pneumothorax; stretch alveoli to get air in)

chest wall or pleural stiffness
- kyphosis
- seizure: all muscles contract
volume work
high metabolic activity

high dead space (PE)
determine if respiratory drive intact
breathing pattern

bedside breathing measurements

measured with respirometer
breathing pattern in determining of respiratory drive intact
mental status
respiratory distress: dyspnea
accessory muscle use
bedside breathing measurements in determining intact resp drive
resp rate: normal about 10 breaths/min

machine vs total breaths

tidal volume : Vt = 5 ml/kg = 350 ml

total minute ventilation : VE = 5 L/min
is muscle strength adequate
general muscle strength
- standing from chair
- turningn over or sitting up in bed
- hair combing, window opening

chest vs ab breathing
- paradoxical pattern = diaphragm fatigue

bedside strength measurements
- vital capacity : VC = 3x tidal volume or > 1 L
- maximal inspiratory P : MIP < -20 cmH2O with MIP meter
is flow work increased?
exam
- wheezing and/or stridor
- thick copious secretions
- pursed lip breathing (to not let air P drop as fast; ppl with flopy airways)
- barrel chest
- long exhalation time (decrease I:E ratio)

PFTs
- decreased FEV (in 1st sec)
- decreased peak exp flow rate (PEFR)
is stretch work increased
exam
- lungs = rales or crackles
- chest wall deformity (scoliosis)
- dullness to percussion
- ab distension, prego, ascites
PFT if stretch work increased
increase restriction; decrease forced vital capacity

increase chest stiffness; decrease static compliance
volume work increased exam
tachypnea: RR > 20
lungs may be clear
CXR may be normal
volume work increased PFT
increase resting minute ventilation : 15-20 L/min

increase dead space : increase Vd/Vt 30% = 50%
- unable to exercise (can't recruit)
- Vd/Vt increase with exercise; should decrease
finding that best characterizes impaired resp drive
apnea with resp acidosis
83 yo female inpt; hip replacement 2 days ago; unarousable for 2 hrs (stroke?); cyanosis, no distress, unresponsive, RR 4; acute respiratory acidosis
normal lung function
hypoxemia = alveolar hypoventilation
elderly pt
recent surgery & narcotics given
comatose, no focal findings, bradypnea
no resp distress
acute alveolar hypoventlation ;normal A-a

= impaired resp drive
- not a lung prob
= brainstem suppression suppression by drugs

support ventilatioin & give narcotic antagonist
narcotic antagonist
naloxone: Narcan
impaired resp drive Ddx
brainstem suppression by drugs or endocrine/metabolic

brainstem damage by trauma or disease (brainstem stroke)

drugs are most common cause of impaired resp drive
18 yomale transferred from another hospital for mechanical ventilation; SOB x 1 wk; cyanosis, confusion, distended neck veins, muscle wasting, accessory muscle use, unable to stand or turn over, RR 32; chronic respiratory acidosis
normal lung function
hypoxemia = alveolar hypoventilation
young person, generalized wkness & muscle wasting
resp distress, tachypnea
chronic alveolar hypoventilation - normal gradient

=poor muscle strength; not a lung problem
- muscular disease

treat precipitating cause
support ventilation :
- acutely or chronically
poor muscle strength Ddx
muscular disease
- drug induced myopathies (steriods, EtOH)
- non drug induced myoopathies : acquired (myositities) or genetic (muscular dystrophy)

neurological disease
- neuronal : polio
- NMJ: myasthenia gravis
tx for poor muscle strength
treat precipitating cause
- correct electrolyte diroders
- treat acute infection
- correct malnutrition

support ventilation
- acutely: oral intubation, ventilator
- chronically: tracheostomy, home ventilator
likely findings in pt with high work of breathing
accessory muscle use
tachypnea
hyperpnea
35 yo male 1 wk hx fever, cough, SOB, worsening SOB on ward x 48 hrs; intubatd after near arrest; resp distress, diffuse crackles; diffuse patch infiltrates on CXR; refractory hypoxemia; normal acid base balance
grossly abnormal lung function
refractory hypoxemia: R-L shunt
young pt, febrile respiratory illness
diffuse alveolar filling pattern on radiograph
shunt typee of hypoxemia

= airspace dz = high work of breathing (stiff)
= primary lung problem (stretch work, not flow)
ARDS: legionella pneumonia
Ddx of high work of breathing
flow work

stretch work
1. parenchymal (airspace disease)
a. alveolar filling process (radiograph)
= cardiogenic pulmonary edema (age)
= non cardiogenic pulmonary edema
= atypical pneumonia
b. interstitial disease
2. pleural disease
3. chest wall disease

volume work
ARDS
a precipitating cause could be legionella pneumonia
refracotry hypoxemia
difuse infiltrates
pulmonary wedge P < 15
stiff lungs: edema

predictable behavior for injured lungs: similar physiology regardless of cause
intrapulmonic shunting in early ARDS
edema & microatelectasis
- perfused, not ventilated
- stiffness = stretch work

arterial becomes venous
- high FiO2 requirement
- PEEP requirement: barotrauma
ARDS tx
Rx underlying cause

minimize O2 consumption
- fully ventilate them
- Rx fever, pain, anxiety
- sedate
- neuromusclar blockade (rarely)

recruit alveoli
- add positive pressure (PEEP) to open up alveoli
what finding best fits with flow work of breathing problem
wheezing
53 yo male with 15 r hx severe asthma; FEV1 28% of predicted 2 yo; increase SOB over last wk; barrel chest, minimal sputum; intubated and bagged (by hand) in ER; hypotensive since intubation; acute on chronic respiratory acidosis; wide gradient
grossly abnormal lung function
COPD
acute worsening
hyperinflation with air trapping on radiograph

high work of breathing
- lung problem
- air trapping worsened by positive pressure ventilation
** Flow work
high work of breathing Ddx
flow work
- upper airway
- lower airway: COPD (bronchospasm moderate, bronchitis, emphysema moderate) & asthma

stretch work

volume work
flow work problem tx
permit more time for exhalation
- increase expiratory time
= decrease ventilator RR
= decrease ventilator tidal volume
= increase inspiratory flow rate

prevent airway closure
- continuous positive airway P : CPAP

drugs
tx drugs for flow work problem
bronchodilators: B agonists

anti inflammatories: steroids

sedatives: benzodiazepines

neuromuscular blockers