Pulmonary I Flashcards
Pulmonary perfusion
movement of mixed venous blood through pulmonary capillary with purpose of exchange between blood and alveolar air
Blood- High volume, low pressure- mean pressure 18
At any time 1/3 of pulmonary vasculature is filled with blood-lung bases, more blood
Mean alveolar pressure
decreased PaO2- shunting blood to areas with increased PaO2
Ventilation
Mechanical movement of air into and out of alveoli
Regulation- CNS, Chemical
Hypercapnic ventilatory drive
Work of breathing
Amount of effort required to overcome the elastic and resistive properties of the lungs and chest wall
Influenced by elasticity (return to normal shape)
Compliance (ability to expand)
High-COPD
Low-PNA, ARDS
Alveolar diffusion
Exchange of O2 and Co2
Oxygen diffuses down the concentration gradient
Remember oxygen bound to heme is…
Useless
Right shift
Oxygen is released more easily decreased pH Increased temp sickle cell pregnancy
Left shift
Oxygen is held on more tightly increased pH PaCo2 decreases decreased temperature hypophosphatemia
Causes of hypoxemia
Hypoventilation (obesity, narcotics, weakness) V/Q mismatch ( R-L shunt Diffusion limitation reduced inspired O2 tension
Normal A-a gradient on room air
7-14
Causes of hypercapnia
Drugs
Diseases of medulla
abnormalities in the spine conducting pathways
Diseases of the neuromuscular junction or respiratory muscles
thoracic cage abnormalities
Large airway obstruction (OSA)
Increased web or physiologic dead space (emphysema)
Dyspnea
Subjective symptom that only patient can perceive
Mechanisms:
Motor
Sensory afferents (chemoreceptors in carotid bodies, mechanoreceptors in the lungs)
integration: efferent-Reafferent mismatch (COPD and asthma patients)
Contribution of emotional or affective factors to dyspnea (anxiety)
Dyspnea and associated disease states
asthma COPD ILD Myocardial dysfunction Obesity Deconditioning HF Pulmonary edema PE
Respiratory dyspnea
Asthma, COPD
Diseases of chest wall
Diseases of lung parenchyma
Cardiac dyspnea
Diseases of the left heart
Ischemic heart disease
Diastolic dysfunction
Diseases of the pulmonary vasculature (PE, PHTN)
Diseases of the pericardium (constructive pericarditis, tamponade)
Other dyspnea
anemia
obesity
deconditioning
medically unexplained
Cough
complex and triggered by sensory nerve endings that can detect both chemical and mechanical exposure
Acute
Less than 3 weeks
infections
aspirations
inhaled chemicals
subacute
3-8 weeks
post viral syndrome
chronic cough
> 8 weeks
cough variant asthma
medications (ACE)
GERD
Hemoptysis
Expectoration of blood from the respiratory tract- must distinguish source (airway, mouth, sinuses, GI)
Causes:
Worldwide- TB
US- Viral/Bacterial PNA
Massive hemoptysis
any amount of bleeding that can compromise airway or hemodynamic stability
Will need ETT for airway protection
Oxygen supplementation
Diffusion gradient- increases it with supplementation (easier diffusion, lowest amount possible for the shortest amount of time)
Goals of treatment SaO2 > 90
Nasal prongs
Assume mouth breathing Oxygen is stored in nasal cavity and drawn down into lungs (Bernouli's principle) Sinuses act as a reservoir 1-6 L Each liter adds 4% O2
Face mask
imprecise
low flow
40-60%
Venturi mask
More precise
uses velocity to create pressure gradient
40-60%
More expensive
Non-rebreather
High flow 11-15 L
Near 100% O2
High flow creates pressure which keeps air from entering from other parts of the mask
Exhaled air into mask move through one way valve preventing rebreathing
Pulmonary function testing
Spirometry
FVC- total exhaled volume after a maximal inspiration and expiration
FEV1- The first exhaled second of FVC
FEV1/FVC
Post bronchodilator testing
after 4 puffs of albuterol and waiting 15 minutes (increase of more than 12% in FEV1 is significant)
Pulmonary function testing
Exhaled NO
Diffusing capacity of carbon monoxide- is used to assess Pulmonary vascular disease
Maximal inspiratory pressures
Bronchial provocation testing- suspect asthma, but no improvement in bronchodilator testing
PFTs and the geriatric patient
TLC usually constant but VC decreases because RV increases
TV may be decreased
Alveoli collapse more easily
Cilia decrease
Decrease in cough and gag reflex
May need more time when performing PFTs with the elderly
PFTs equation variables to figure out normal lung volumes
height
Age (declines with age)
Gender
Race (black man has shorter torso so shorter lungs than white man)
What is abnormal value for FVC
less than 80% of the predicted normal value given the 4 variables
Two problems with lungs found on PFTs
Restriction- problem with volume of lungs
Obstruction- problem with airways
FVC stands for
Forced Vital Capacity
How do you perform an FVC
take a deep breath in and blow it out as fast and as completely as possible
The initial flow of the FVC comes from
The large airways
The latter flow of the FVC comes from the
Small airways, alveoli
FVC is
The volume of air that you can move in a forced manner
FVC is decreased with
Restriction
Restriction is caused by
Fibrosis (intrinsic) scoliosis (extrinsic) neuromuscular disease (ex) obesity (ex) Pulmonary edema (in)
How do we know if the number is normal or low?
Take the four variables and get a number, take the FVC and divide by the “normal” for the 4 variable, If 80% of predictive or better than you are normal. < 80% of predictive then you have a restrictive lung disease
FEV1 stands for
Forced expiratory volume in 1 second
FEV1 is a volume but shows
a flow rate
FEV1- the more volume you can get out in 1 second the better the…
flow
Small airways are…
effort independent
you can blow as hard as you want but you can’t effect the flow coming from the small airways
FEV1/FVC- normal
70%
< 70% of FEV1/FVC shows
Obstruction
On inhalation, intrathoracic airways get…
bigger
On exhalation, intrathoracic airways get…
Smaller
On inhalation, extrathoracic airways get…
smaller
On exhalation, extra thoracic airways get…
bigger
Obstructions always manifest themselves when the airways are…
small
therefore obstructions manifest intrathoracic on… and extrathoracic on…
exhalation
inhalation
What is the DlCO?
A way of measuring the cross sectional surface area of the lungs and capillaries
High DLCO is
normal > 80%
Low DLCO is
marker of low pulmonary surface (architectural destruction) area such as
COPD, Emphysema, Pulmonary HTN, Fibrosis
or marker of extrinsic problem such as scoliosis, obesity, chest wall abnormality
How can you tell the cause of the low DLCO?
By looking at Va (alveolar ventilation) if the alveolar ventilation is normal than it is caused by architectural destruction and ventilation problem
How to differentiate asthma from COPD
both will have low FEV1/FVC
but for COPD the DLCO will be low while it will be normal or high in asthma
Interpreting PFTs
- FVC is it > 80% of predicted (yes, no restriction), (no, then you have restriction or obstruction with air trapping.)
- Is FEV1/FVC > 0.7? (yes, no obstruction), (no, obstruction)
- Is TLC > 80% of predicted? (Yes, obstruction) (no, restriction)
Gold stages look at…
FEV1 only
Gold stage I
80-100
Gold stage 2
50-80
Gold stage 3
30-50
Gold stage 4
0-30
respiratory failure with an elevated PCO2 level
Also need to classify with Obstruction
Reactivity or not
How to determine reactivity
Bronchodilator testing
If FEV1 or FVC >12% improved and 200 ml than there is reactivity
DLCO > 80% of predicted?
Yes- normal membrane surface area
No- abnormal membrane surface area
DLCO/Va > 80% of predicted?
Yes- Extrinsic lung disease
No- Intrinsic lung disease
Asthma is a
chronic inflammatory condition of the airways, common in young males, adult females
Atopy is..
allergies and are a major risk factor for asthma
Asthma is diagnosed…
with symptoms and objective measurement of lung function
Spirometry on asthma shows…
airflow limitations with reduction in FEV1, FEV1/FVC ration and peak expiratory flow
Asthma s/sx
episodic wheezing chest tightness cough increased sputum production nocturnal worsening
ABG finding that could show impending respiratory failure
PCO2 rising or normalizing
Asthma PFTs…
decrease of more than 20% of normal is asthma exacerbation.
PEF thats greater than 50% of baseline is considered a severe attack
Asthma CXR…
CXR will be normal, diaphragmatic flattening shows chronic condition
Asthma exacerbation classifications
mild, moderate, severe, respiratory arrest
Medications for long term asthma control…
inhaled corticosteroids systemic corticosteroids long acting/short acting beta-2-agonists Cromolyn and Nedocromil Inhaled long acting anticholinergic phosphodiesterase inhibitors leukotrine modifiers immunomodulators
Asthma medications for quick relief
Beta-adrenergic agonists
Anticholinergic agents
corticosteroids
All asthma patients should be immunized with
pneumococcal vaccination, annual influenza vaccine recommended
Mild asthma exacerbation
minor changes in PEF (usually more than 80%)
SABA a mainstay of therapy at increased doses
Consider PO steroid in patients on inhaled steroid (7 day coarse)
Moderate asthma exacerbations
correct hypoxemia, reverse obstruction and reduce likelihood of recurrence
SABA+systemic corticosteroids
think peak flow less than 70=steroids
how much FEV1 improves after 30 minutes correlates with severity of exacerbation
Severe asthma exacerbations
Life threatening
Oxygen, SABA, Steroids
+ Ipratropium
IV magnesium-2 g over 20 minutes, smooth muscle relaxation
NO mucolytics (can worsen cough and obstruction)
Avoid anxiolytics
Abx when indicated, not given empirically
Asthma when to refer
Atypical presentation
complicated comorbid problems
poor response to therapy
On high dose steroids
Not meeting goals after 3-6 months of treatment
More than 2 course of oral steroids in 2 months
Life threatening asthma exacerbation or hospitalization in last 12 months
COPD is
a disease state characterized by the presence of airflow obstruction due to chronic bronchitis or emphysema
It is progressive, most patients have features of both
Risk factors- cigarette smoking, environmental exposures, hereditary factors
COPD s/sx
4th-5th decade of life
excessive cough, sputum, SOB
Late stages- pneumonia, pulmonary htn, cor pulmonale, chronic respiratory failure
Type A COPD
"Pink puffers" c/o dyspnea less coughing thin, weight loss accessory muscle use chest quiet oxygenate fine CXR-hyperinflation, flattened diaphragm TLC-increased
Type B COPD
"Blue Bloaters" loud chronic cough sputum chest infections Mild dyspnea overweight cyanotic peripheral edema noisy chest reduced PaO2 CXR- interstitial markings TLC- normal
Spirometry is required to make the diagnosis of…
COPD
COPD symptoms
progressive dyspnea cough sputum production wheezing chest tightness ankle swelling syncope
COPD spirometry
early-abnormal closing volume and reduced mid expiratory flow rate
FVC-reduced
RV-increased
FEV1 and FEV1/FVC- decreased later in disease less than 0.7 for diagnosis
Classification of severity of airflow limitation in COPD
GOLD 1: mild FEV1 > 80
GOLD 2: moderate 50-80
GOLD 3: Severe30-50
GOLD 4: Very severe < 30
Alpha-1 antitrypsin deficiency screening
All patients with COPD diagnosis
typically < 45 years with pan lobular basal emphysema
Prevention and maintenance therapy for COPD
Smoking cessation is key
safety of e-cigarettes as a smoking cessation aid is uncertain at this point
Pharmacologic therapy to reduce COPD symptoms, frequency and severity of exacerbations
All therapy should be individualized
Inhaler teaching
Flu and PNA vaccine
Pulmonary rehabilitation
Long-term O2 therapy
Offer palliative approaches in advanced COPD
Pharmacologic treatments of Alpha-1 antitrypsin disease
IV augmentation therapy may slow down the progression of emphysema
Pulmonary rehabilitation in COPD patients..
improves dyspnea, health status and exercise tolerance in stable patients
reduces hospitalizations among patients who have had a recent exacerbation
Goals for treatment of stable COPD
Relieve symptoms, Improve exercise intolerance, improve health status, reduce risk of disease progression, prevent exacerbations, reduce mortality
Preferred treatment for patients with stable COPD
Long-acting beta agonists
Long-acting muscurinic agonist are preferred over short acting agents except for in patients with only occasional dyspnea
inhaled corticosteroids are only recommended in association with a LABA for patients with a history of exacerbations
Group A patients pharmacologic treatment
A bronchodilator- All group A patients should be offered bronchodilator treatment based on its effect on breathlessness. This can either be short or long acting
Group B patients pharmacologic treatment
Initial therapy should consist of a long acting bronchodilator.
LAMA or LAMA/LABA if having severe breathlessness
Group C patients pharmacologic treatment
LAMA started first, then step up to LAMA/LABA or LAMA/ICS (alternative)
Group D patients Pharmacologic
LAMA/LABA to start- if continuing to have problems, LAMA/LABA/ICS, then you can do additional therapies from there
Consider macrolide in former smokers
Nonpharmcologic treatment in COPD
Education and self management Physical activity Pulmonary rehabilitation Exercise training Self management education End of life and palliative care nutritional support Vaccination Oxygen therapy
Oxygen therapy for COPD
Long term oxygen is indicated for stable patients PaO2 less than 55, < 88%. Prescribe O2 to keep Sat > 90%.
Monitoring and follow up for patients for COPD
Spirometry should be preformed once a year
Information on symptoms should be collected at each visit (cough, sputum, breathlessness, fatigue, activity limitation and sleep disturbances)
Exacerbations (frequency, severity, type)
Smoking status
Management of COPD exacerbations
can be precipitated by several factors ( most common are respiratory tract infections, viruses)
SABD are recommended as the initial bronchodilators to treat an acute exacerbation
Start maintenance therapy as soon as possible before discharge
systemic corticosteroids can improve lung function, duration of therapy 5-7 days
Antibiotics when indicated
COPD classification and treatment
Mild- SABD
moderate- SABD plus antibiotic and/or oral corticosteroids
Severe- patient requires hospitalization
