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61 Cards in this Set
- Front
- Back
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What clinical symptoms distinguish acute respiratory failure
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PaO2 < 60 torr with no supplemental oxygen and no R-L shunt
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What clinical symptoms distinguish acute respiratory failure (2nd def)
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PaCO2 > 50 torr with absence of respiratory compensation for metabolic alkalosis and hypoventilation
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How can acute respiratory failure be distinguished from hypoventilation
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by looking at the PAO2 and PaO2 gradients - PaO2 < 60 torr
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How can acute respiratory failure be distinguished from chronic respiratory failure
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...by comparing the PaCO2 and pH
- in acute - PaCO2 is elevated and pH is acidotic - in chronic - pH is normal due to metabolic compensation |
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Respiratory failure is usually accompanied by a decrease in
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FRC and lung compliance
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Respiratory failure is usually accompanied by an increase in
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PA pressures
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Respiratory failure is usually accompanied by
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pulmonary hypertension
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ARDS is characterized by
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acute alveolar damage, leaking protein rich edema into the alveoli
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What is the result of ARDS leaking
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noncardiogenic pulmonary edema
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Causes of ARDS can be due to
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aspiration of gastric contents
pneumonia pulmonary contusions indirect injury r/t sepsis trauma with severe shock multiple blood transfusions cardiopulmonary bypass |
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What are clinical signs of ARDS
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arterial hypoxemia resistant to supplemental oxygen
CXR - pulmonary edema (cotton, fluffy) |
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ARDS pt has
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poor lung compliance
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ARDS may progress to
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pulmonary fibrosis
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Three treatment goals for ARDS
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1. correct hypoxemia - supplemental oxygen for PaO2 > 60 torr (SpO2 > 90%)
2. excessive CO2 3. provide patent ariway |
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ARDS pt - why is pushing PaO2 above 80 torr of little benefit
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per oxygen dissociation curve, HGB is all loaded up - minimal bang for the buck
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ARDS pt - what may be required to get positive pressure
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intubation
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ARDS pt - what may be needed to get rid of CO2
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mechanical ventilation
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ARDS pt - what two things will have to be changed to attain goal PaO2/SpO2
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PEEP and FiO2
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ARDS pt - what is the best method for increasing FiO2 and PEEP to achieve oxygenation goals
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alternate - 0.3 FiO2 - 5 PEEP - 0.4 FiO2 - 8 PEEP - 0.4 FiO2 - ,,, etc
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ARDS pt
What is more toxic to alveolar membranes - high oxygen concentrations, high volumes (10-12 ml/kg), or high pressures (30 cmH2O) |
all three are damaging
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ARDS pt - as alveolar resistance increases, the volume of a breath delivered will follow
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the least path of resistance - filling alveoli that are already open
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ARDS pt - recommendations to ventilate at what volume and pressure
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5-8ml/kg, 30cmH2O
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ARDS pt - ventilating at relatively lower volume (5-8) and pressure (30) leads to
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permissive hypercapnea
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ARDS pt - why do high pressures and volume cause damage
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the tissue is noncompliant
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ARDS trial study
1st group rec'd 12 ml/kg volumes 2nd group rec'd 6 ml/kg volumes What are 3 take home messages |
1. mortality and vent free days was better with low volumes and higher rates
2. lower tidal volumes, despite high vent pressures and high FiO2 resulted in less interleukin 6 (inflammation) in alveoli and lung tissue 3. excessive stretch AND ALSO collapsing and reopening could be damaging - the group with higher tidal volumes did not require as much pressure to oxygenate |
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ARDS trial study
Pts who received lower volumes had |
better mortality rates and vent free days
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ARDS trial study
Pts who received lower tidal volumes had less |
interleukin 6 - inflammation in alveoli and lung tissue
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ARDS trial study
Not only does excessive stretch damage lung tissue but so does |
constant collapsing and opening noncompliant tissue (I think of fatigue in a metal bar - it will eventually break)
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ARDS trial study
Excessive stretch of alveoli is thought to cause |
ventilator induced lung injury
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ARDS trial study
What is thought to benefit small airways and alveoli by decreasing excessive alveolar stretch |
control of plateau pressure (PPV)
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ARDS trial study
Peak pressure is measured in the |
major airways
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ARDS trial study
Peak pressure in the major airways reflects |
airway resistance
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ARDS trial study
In severe asthma there is a large gradient between the |
peak pressure (high) and plateau pressure (normal)
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ARDS trial study
In PC ventilation, the pressure limit is usually the |
plateau pressure - due to the dispersion of the gas in inspiration
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ARDS trial study
In AC ventilation, the pressure limit pressure measured by the ventilator is |
peak airway pressure - pressure at level of major airways
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ARDS trial study
to know the real airway pressure, the plateau pressure applied to alevolar level |
the volume breath must be made to simulate a pressure breath - an inspiratory hold of 0.5-1s is applied, and the airway pressure, from the initial peak, drops down to a plateau. The hold represents no flow
THIS ONE PAGE IS TOUGH TO MAKE CARDS FOR... |
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LOOK AT PAGE 7 FOR GRAPHS
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LOOK AT PAGE 7 FOR GRAPHS
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Tidal volumes are based on
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ideal body weight
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ARDS pt
Since lungs are noncompliant, they will resist inflation - so need to set |
longer I times and lower E times
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ARDS pt
Protocol ventilation settings What ventilator mode |
volume assist control
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ARDS pt
Protocol ventilation settings What tidal volume |
<6ml/kg - predicted body weight
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ARDS pt
Protocol ventilation settings What plateau pressure |
< 30cm H2O
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ARDS pt
Protocol ventilation settings What pH goal |
> 7.30 if possible
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ARDS pt
Protocol ventilation settings What ventilation set rate |
6-35/min (adjust for pH)
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ARDS pt
Protocol ventilation settings What I:E |
1:1-1:3
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ARDS pt
Protocol ventilation settings What oxygenation goal |
> 60 torr, ~90%
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ARDS pt
Protocol ventilation settings When/how wean |
by pressure support, when FiO2/PEEP < 40/8
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ARDS pt
3 Other management tools |
sedation - breathe the way you want
barotrauma - with higher PEEPS paralysis - don't want to use energy to breathe |
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Pulmonary hypertension defined
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abnormal elevation of the pressure in the pulmonary circulation caused by the constriction of the blood vessels that supply blood to the lung
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Two symptoms of pulmonary htn
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SOB, dizziness
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Causes of pulmonary htn - heart
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LV failure
valve disorders congenital anomalies myocardial dysfunction - MI or cardiomyopathy |
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Causes of pulmonary htn - lung
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infections
drug induced (bleomycin) toxins COPD embolism OSA scleorderma |
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The result of chronic hypoxia is
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cor pulmonale
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Cor pulmonale is
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pulmonary htn r/t underlying lung disorder in which the RV of the heart becomes enlarged and thickened, eventually resulting in heart failure
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How does cor pulomonale occur from hypoxia
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1. pulmonary arteries constrict and thicken in response to low oxygen levels
2.the thickening narrows passageways for the blood 3. narrowing increases pressure in pulmonary arteries |
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Cor pulmonale
Once pulmonary htn develops, |
the right side of the heart has to work harder to compensate - enlarges and thickens
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Cor pulmonale
The failing right ventricle places a person at risk for |
pulmonary embolism b/c blood flow is slow and pools in legs - clots may form and travel and lodge in the lungs = bad
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Pickwickian syndrome is sometimes called
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obesity hypoventilation syndrome (OHS)
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Pickwickian syndrome - what is the problem
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hypoxemia + hypercarbia = pulmonary vasoconstriction (pulm htn)
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Pickwickian syndrome is associated with
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obstructive sleep apnea
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Pickwickian syndrome - symptom
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somnolent during the day
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