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81 Cards in this Set

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tension pneumothorax
1)clinical diagnoses
2)In a chronic condition, airways don't re-expand spontaneously because of scarring
Underventilation lung due to pressure from mechanical ventilation
1)susceptible to puncture
2)hypotensive
3)tachycardic
4)hypoxic
5)code
PCO2 of 100 in a COPDer
Patients can have PCO2's of up to 100, and, as long as they crept up slowly, can still be talking
PaO2
tension of oxygen in an arterial blood gas sample
advantages to the shape of the O2 dissociation curve
1)In the physiologic range of 70-100, significant changes in the arterial 02 do not affect the oxygen saturation
PaO2 55-60
1)indications of giving the pt. oxygen to prevent the complications of hypoxemia
Factors affecting the Oxyhemoglobin dissociation curve
1)Temperature
2)2,3 DPG
3)PCO2
4)ph
Chronic hypoxemia and red blood cell production
1) stimulus goes out the kindeys to put out erythropoeitin
2)Eth. stimulates production of RBC's
Anemia and PO2 and O2
Assuming the lungs are normal, the PO2 and O2 will be normal
Partial Pressure of O2 in the lungs
As the O2 gets to gas exchange, it encounters O2, and the partial pressure of O2 decreases
Before O2 gets to the systemic arteries
1) Some ventilation/perfusion inequalities
2)1-2% of the blood is shunted to the left side without going through the lung, causing alveolar and oxygen tensions to be different
Alveolar air equation
Allows us to estimate PO2 in the alveolus
R in the aveolar air equation
1)represents the respiratory exchange ratio
2)Ratio between the volume of CO2 added to the alveolus and the volume of O2 removed from the alveolus
R=VCO2/VO2
Used to correct for the fact that more O2 is taken up than CO2 is excreted back into the airways (0.8)
As PCO2 increases
Alveolar O2 decreases
P(A-a)O2 over age
normally increases with age, 2.5 +age/5
PO2 for our altitude
122
PCO2 at our altitude
36-39
Normal values for PaO2
65-75
causes of hypoxemia
1)hypoventilation
2)ventilation/perfusion mismatch
3)shunt
V/Q mismatch
Most common cause of hypoxemia in pts with COPD
Hypoventilation
There is no change in A-A difference
v/q mismatch and A-a diff
There will be a a-A difference of more than to 10, using the formula for age
COPD PaO2
1)There will be a PaO2 of 50-60
Widened A-a gradient
Both shunt and V/Q mismatch results in a widened A-a gradient
Physiologic consequences of chronic hypoxemia
1)pulmonary hypertension
2)erythrocythemia
3)CNS dysfunction
4)Decreased exercise tolerance
5)Cor pumonale
6)shortened survival rate
Hypoxemia in lung vessels
1)Causes vasoconstrictionb
2)remodeling
Failure of R VENTRICLE
Patients develop edema
neck veins distended
Cor pulmonale
Due to pulmonary hypertension
Liquid Oxygen system
1)High flow rates
2)Oxygen coming out is 100%
COPD
Leading cause of morbidity and mortality
Natural History of COPD
15-20% of smokers develop COPD
definition of COPD
A disease state characterized by airflow limitation that is not fully reversible
Genetic predispositions to COPD
linked to enzymatic deficiency
Subcategories of COPD
1)chronic bronchitis
2)emphysema
3)Asthma
Chronic bronchitis is a _____
Clinical Diagnoses (must have symptoms for 3 months out of the year for two consecutive years)
Emphysema
Pathological Diagnoses
Alveoli walls are destructed. Visible on CT scan
Asthma
1)Chronic inflammatory disease
2)Characterized by the increased responsiveness of trachea and bronchioles to different stimuli
Pts who show complete responsiveness to a bronchodilator
Do not have COPD
Other causes of COPD
1)tobacco
2)smoke inhalation
3)chemical inhalation
4)Childhood infections
5)deficiency of alpha one antitrypsin
Areas of body affected by COPD
1)central airways
2)peripheral airways
3)lung parenchyma
4)pulmonary vasculature
Changes brought about by COPD
1)ciliary dysfunction
2)increased sputum production
3)loss of airway elasticity
4)pulmonary hyperinflation
5)pulmonary hypertension
Clinical Features of COPD
20 cigarettes a day for 20 or more years
Clinical symptoms of COPD continued
-Acute bronchitis every winter
-upper respiratory depression that doesn't go away
-prescriptions don't help
-acute phase 50's, present with SOB in 60's
-weight loss
-muscle wasting
-headache/delirium
-right side heart failure/cor pulmonale
Why do COPDers have right sided heart failure
Because, when alveoli get destroyed, there is an increase in interstitum. Pulmonary pressures increase.
COPD lung morphology
Increase in total lung capacity, and increase in functional residual capacity
COPD CT scan
shows bullae
COPD FEV1 with bronchodilator
1) at risk/mild--80 percent or less
2)moderate-50 to 80
3)Severe--less than 30
Alpha-one antitrypsin disease
1)Genetic disease
2)people diagnosed with COPD at a young age
3)runs in families
Average rate of capacity loss in a smoker
1)20-30 ml per year
FVC
Total volume of air that can be exhaled, from maximal inhalation to maximal exhalation
Short acting bronchodilators
increase exercise tolerance
Long acting bronchdilators
1)Improve health status
2)reduce symptoms
Anticholinergics
1)reduce exacerbations
2)reduce hospitalizations
Steroids
1)Act at multiple points in the inflammatory cascade
2)don't work as well in COPD as they do in asthma
Pulmonary Rehabilitation
1)Increases exercise tolerance
2)Improves dyspnea
3)Improves muscle tone
Nutrition and COPD
muscle wasting due to increased respiratory effort
--significant weight loss=pt. losses 5 percent of their weight in one month, or greater than 10 percent of their weight in six months
Surgical options for COPD patients
1)bullectomy
2)lung volume reduction sugery
3)lung transplant(less than 55 years old, have alpha-one antitrypin deficiency
4)must have 60% of FEV1 before surgery, to guarantee 40% after
Exacerbations of COPD
1)increased mucus production
2)dyspnea
3)fevers(pneumonia)
Inpatient therapy for COPDers
1)steriods
2)antibiotics
3)nebulizers
4)short acting bronchodilators(beta 2 agonist)
5)CXR
6)ABG gases (ph, oxygenation)
BIPAP helps with
1)hypercapnia
2)respiratory acidosis
3)CHF
4)COPD
Contraindications for BIPAP
1)facial fractures
2)excessive secretions
3)comatose,unconscious,unable to follow directions
Pressure support increases
1)Tidal volume
2)keeps airways open
Prolastin augmentation therapy
1)slows rate of decline in patients with alpha one antitrypsin deficiency
2)improves survival rate in patients with moderate airflow obstruction
Causes of restrictive lung disease
1)alteration in lung parenchyma
2)disease of the chest wall
3)disease of the pleura
4)disease of the neuromuscular apparatus
Pathpophysiology of restriction
1)Parenchymal destruction
2)Excessive elastic recoil of the lung
3)diease of the pleura
4)reduced FEV1
5)Arterial hypoxemia due to VQ mismatch
6)yperventilation at rest
Definition of asthma
chronic inflammatory disorder where many cells play a role
cells that play a role in asthma
1)mast cells
2)eosinophils
3)T lymphocytes
Symptoms of asthma
1)Wheezing
2)SOB
3)Chest tightness
4)Coughing at night, during morning
Mediators in asthma
1)Histamine
2)Activating Factors
3)Cytokines, such as interleukin three and five
Bronchial hyperresponsivenes in asthma
1)Exaggerated response to allergens, histamine, methylcholine, cold air, and environmental irritants
Elements of airflow obstruction
1)Acute bronchoconstriction
2)mucus plugging
3)bronchial wall edema
Lung remodeling
1)Smooth muscle hypertrophy
2)Lung loses recoil features
Risk factors for asthma
1)Genetics
2)Sex
3)Race
4)Envinronmental Factors
Details of Genetic Risk Factors for asthma
Short arm of chromosome five shows alterations. Pts. who have asthma have high IGE. Only in select groups of patients.
Sex and asthma
In childhood, more prevalent in males. In adolescence, more prevalent in females.
Race and asthma
More common in African Americans
Environmental Factors
Allergens, dust mites, cockroaches, pollen, industrialized cities, air pollution.
Other respiratory infections associated with asthma
1)Chylamidia
2)mycoplasma
Miscellanous Asthma correlates
1)weight
2)antioxidants
Clinical Presentation of asthmatics
1)wheezing
2)Hyper-resonant