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86 Cards in this Set

  • Front
  • Back
list ways to detection hypoxemia
PaO2, O2 sat, ABG's
reduction in blood O2 levels i known as
hypoxemia
which would not directly result in insufficient O2:
diseases of the lung, neurologic disorders, cardiac disorders, insufficient O2 in the air, breathing into a bag
breathing into a bag. The rest do
Middle aged Pt presents to the ER combative, but uncoordinated. He is easily agitated by your questions. Blood test rules out alcohol. What is your next step?
Place pt on O2, symptoms match severe hypoxia
what is dangerous about chronic hypoxia.
Among other things, that is insidious and you often don't realize you have a problem.
List the four mechanisms we have to compensate for hypoxemia
increase rate and depth of breathing
pulmonary vasoconstriction (directs blood to areas that are getting O2)
Increase in Erythropoetin which increases RBCs
shift in O2 curve to the right
Pt presents with cyanosis of the mucous membranes and skin. Pa O2 is 96. What do you test for.
Polycythemia may present as cyanosis without hypoxemia
the gold standard for measurement of O2, CO2, and pH
Arterial samples
why would you choose to use pulse oximetry instead of ABGs
pulse ox is less invasive and can give continual readings
Pt brought to ED by ambulance. Was pulled from a burning house. No major burns, but smoke inhalation. PF ratio is 190. What do you suspect?
Normal PF ratio is 300. Lower PF ratios are associated with acute lung injury and ARDS. Pt probably has burns on her lungs due to high temp of smoke inhaled.
What is the first treatment for hypoxemia? what is the hallmark?
Find the cause and remove
then Oxygen (hallmark)
Why do we not leave pts on long term 100% O2
May cause symptoms and lung injury
when do you see hypercapnia with hypoxemia
hypoventilation
What may cause hypercapnia
increased metabolism (fever, exercise), underlying renal disease (disruption of buffer system).
how can O2 use in hypercapnia lead to coma?
increased levels of CO2 depress the brains natural stimulus to breath. If this happens enough pt will become hypoxemic, which will iniate a different drive to breath. If you give O2 thus taking care of the hypoxemia. You take away that secondary drive to breath, but the first one is still gone because the pt is still hypercapnic. Resulting in NO drive to breath
Match the disorder with its impact on the lung
Pneumothorax Collapse
Atelectasis Compression
Pleural effusion Restriction
pneumothorax and PE both compress the lung, one could argue restricting its movement
Atelectasis is a collapsed segment of the lung.
Pt experiencing pain with breathing. Upon exam you do not hear good breath sounds and is hyper-resonant upon percussion. Chest X-Ray shows tracheal shift
pneumothorax
The pleura of the lungs has two layers with a serous fluid between them. Name them and give location
parietal pleura- lines inner chest cavity
visceral pleura- covers lung
Pt presents with "sharp localized" pain upon breathing. Has history of URI w/n one week, no Hx of trauma. What do you suspect, and how do you treat? what if they did have present HX of trauma?
Pleurisy, Nsaid or indomethacin
if HX of trauma would need to rule out chest pain due to rib fractures
Epidemic pleurodynia is also known as... and is due to what bug
Von Holms disease
the group B coxsackievirus
leading causes of pleural effusion in the US
heart failure, pneumonia, cancer
identify the 5 mechanisms associated with PE
increased capillary pressure
increased cap permeability (inflammation)
decreased colloidal pressure (hypoalbumin, nephrosis)
increased negative pressure (atelectasis)
impaired lymphatic drainage (obstruction often cancer)
pt presents with chest pain, dyspnea, fever. Exam: dullness to percussion, decreased breath sounds. Egophony above the dullness. What tests do you need to order? If tests confirm your suspicion what is the treatment?What does egophony above dullness suggest.
Chest X-ray- looking for fluid to blunt costophrenic angle (250mL)
Drain is enough fluid is present
egophony above the effusion means that that area has succumbed to atelectasis
Why do you drain an PE
for both treatment and as a diagnostic measure. Type of fluid can tell you origin of PE.
PE fuid drained has protein level of 2.0 g/dl cholesterol level of 40 mg/dl protein ratio (fluid/serum)of .4 and LDH ratio of .38, pH 7.48
What is the etiology of this fluid?
Transudate, most likely from CHF
PE fluid drained has protein level of 3.6 g/dl, cholesterol level of 52mg/dl, protein ratio (fluid/serum)of .6 and LDH ratio of .52, pH 7.63
Exudate, could be infection
Exudates in PE flid are commonly associated with what
infection, infarction, malignancies, and connective tissue disorders
Pt has recurrent PE. you treat by instilling tetracycline and talc between the pleura, causing adhesion of the two layers. what procedure did you just perform
pleurodesis
Pt is 65 yo male with emphysema. Has new pain and difficulty associated with breathing. Exam yields hyper-resonance over left lower lobe
spontaneous pneumothorax due to rupture of emphysematous bleb
15 y/o male, has pain and difficulty associated with breathing.Has had this multiple times before. Exam yields hyper-resonance over right lower lobe. What is your diagnosis and patient education
spontaneous catamenial pneomothorax

avoid pressure extremes (planes, scuba) and don't smoke
some common causes of traumatic pneumothorax are knife wounds and rib fractures. what are some uncommon causes
esophogeal perforation (watch for in severe GERD pt) and iatrogenic
Pt presents to ER with stab wound right anterior chest just below 3rd rib. Pt is tachycardic, cyanotic, and dyspnic. Breath sounds are very diminished. Chest Xray shows shift of heart and atelectasis of L lung. DX and treament
tension pneumothorax, large bore needle into area, if sucking cover with vaseline guaze and occlusive dressing
When can primary atelectasis occur
only in newborns that have never ventilated that lung
incomplete expansion of lung
atelectasis
list some causes of atelectasis
airway obstruction, lung compression due to pneumothorax or PE, inability ot take deep breaths, sedation
Pt is in postop after GI surgery. Nurse notices fever and calls you over. Upon exam lungs are dull to percussion, and tactile fremitus is increased
DX and treatment
atelectasis, encourage pt to take long deep breaths, reinflation of lung may be necessary
list some obstructive airway disorders
asthma, COPD, bronchiectasis, cystic fibrosis
what is characteristic of all obstructive disorders
all decrease ventilation in the airways
what is the approximated prevelance of asthma
1:15
"a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role, in particular mast cells, eosinophils, t lymphocytes, and epithelial cells."
asthma
some common causes of traumatic pneumothorax are knife wounds and rib fractures. what are some uncommon causes
esophogeal perforation (watch for in severe GERD pt) and iatrogenic
Pt presents to ER with stab wound right anterior chest just below 3rd rib. Pt is tachycardic, cyanotic, and dyspnic. Breath sounds are very diminished. Chest Xray shows shift of heart and atelectasis of L lung. DX and treament
tension pneumothorax, large bore needle into area, if sucking cover with vaseline guaze and occlusive dressing
When can primary atelectasis occur
only in newborns that have never ventilated that lung
incomplete expansion of lung
atelectasis
list some causes of atelectasis
airway obstruction, lung compression due to pneumothorax or PE, inability ot take deep breaths, sedation
Pt is in postop after GI surgery. Nurse notices fever and calls you over. Upon exam lungs are dull to percussion, and tactile fremitus is increased
DX and treatment
atelectasis, encourage pt to take long deep breaths, reinflation of lung may be necessary
list some obstructive airway disorders
asthma, COPD, bronchiectasis, cystic fibrosis
what is characteristic of all obstructive disorders
all decrease ventilation in the airways
what is the approximated prevelance of asthma
1:15
"a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role, in particular mast cells, eosinophils, t lymphocytes, and epithelial cells."
asthma
this reponsse in asthma usually occur w/n 10-20 minutes of inhaled irritant and is most likely due to the release of mast cells
early/acute phase response
can be modified by b- agonists (bronchodilators)
this phase of asthma occurs 4-8 hours after irritant, but may last for days. Due to migration of inflammatory cells and epithelial injury
late phase response
this test should be performed on all asthma pts.
This test should be performed before and after bronchodilator use
spirometry
Forced Expiratory Volume
7 yo presents with wheezing and dyspnea after playing outside. Upon visual examination you notice use of accessory muscles for beathing and slight cyanosis
asthma
potentially fatal manifestation of acute asthma where there is lack of response to treatment resulting in cyanosis, hypoxemia, hypercarbia, and acidosis. Pt should be admitted to ICU
status asthmaticus
list some clinical management issues with asthma
EDUCATION, training in proper technique and timing, should have peak flow meter, keep daily diary, and contacts in case of emergency, flu and pneumonia shots, avoid allergens
progressive, non-reversible obstructive disease most often caused by smoking
COPD
36 yo pt diagnosed with emphysema. Pt has never smoked. diagnosis and treament
alpha 1 antitrypsin (autosomal recessive)
weekly IV enzyme replacement
the permanent enlargement of air spaces distal to the terminal bronchioles, not fibrosis
emphysema
clinically productive cough for 3 months in each of two sucessive years
chronic bronchitis
this reponsse in asthma usually occur w/n 10-20 minutes of inhaled irritant and is most likely due to the release of mast cells
early/acute phase response
can be modified by b- agonists (bronchodilators)
this phase of asthma occurs 4-8 hours after irritant, but may last for days. Due to migration of inflammatory cells and epithelial injury
late phase response
this test should be performed on all asthma pts.
This test should be performed before and after bronchodilator use
spirometry
Forced Expiratory Volume
7 yo presents with wheezing and dyspnea after playing outside. Upon visual examination you notice use of accessory muscles for beathing and slight cyanosis
asthma
potentially fatal manifestation of acute asthma where there is lack of response to treatment resulting in cyanosis, hypoxemia, hypercarbia, and acidosis. Pt should be admitted to ICU
status asthmaticus
list some clinical management issues with asthma
EDUCATION, training in proper technique and timing, should have peak flow meter, keep daily diary, and contacts in case of emergency, flu and pneumonia shots, avoid allergens
progressive, non-reversible obstructive disease most often caused by smoking
COPD
36 yo pt diagnosed with emphysema. Pt has never smoked. diagnosis and treament
alpha 1 antitrypsin (autosomal recessive)
weekly IV enzyme replacement
the permanent enlargement of air spaces distal to the terminal bronchioles, not fibrosis
emphysema
clinically productive cough for 3 months in each of two sucessive years
chronic bronchitis
most common type of emphysema affecting the bronchioles of the central lobules. most commonly seen in males with high pack years
centrilobular emphysema
emphysema affecting the peripheral alveoli first then extending centrally. Characteristic of alpha 1 antitrypsin deficiency
panacinar emphysema
chronic inflammation of the bronchial tree with thick sputum progressing to purulent sputum. generally caused by smoking. x-ray may reveal blebs and increase in bronchovascular markings
chronic bronchitis
emphysema pts who overventilate to keep good ABGs. develop barrel chest
"pink puffers"
emphysema pts who cannot compensate via hyperventilation and become cyanotic. more likely to develop pulmonary hypertension and polycythemia
"blue bloaters"
pt presents with hx of cough, cputum, dyspnea and smoking. Physical reveals hyper-ressonant percussion, distant breath sounds, and pursed lip breathing, Xray reveals flattened diaphragm and loss of lung markings. What do you suspect and how would you definatively diagnose
COPD
spirometry
classic FEV1/FVC ratio for COPD
< .7
FEV1 of <50% = SEVERE
total lung capacity, residual volume, and functional residual capacity all increase or decrease with advanced COPD
increase
1st treatment for COPD
stop smoking
list some treaments for COPD
flu and pneumonia vac, oxygen (1-2 L/min when Po2 below 55 mmHG), bronchodilators, maybe theophylline, surgery (take out parts or transplantation)
uncommon respiratory disorder characterized by dilation of the bronchi secondary to frequent infection or inflammation
bronchiectasis
pt presents with cough, foul smelling sputum, weight loss and clubbng. Has hx of recurrent URI.
dx and tx
bronchiectasis
postural drainage, treatments for COPD, prophylactic antibiotics
the most common cause of COPD in children. caused by deficiency in chromosome 7. moms diagnose by salty kisses
cystic fibrosis
what is the most common infecting agent exascerbating cystic fibrosis
pseudamonas
while screening for trypsinogen can be done, what is the gold standard for cystic fibrosis
sweat test
this organ is almost always involved in cystic fibrosis (besides the lungs)
pancreas