Pulmonary Flashcards
Basic COPD pathology
Something is obstructing airflow. This obstruction is caused by either chronic bronchitis or emphysema.
Overall, this obstruction is progressive, but may be partially reversible. May be associated with hyper-reactivity
Basic gas problems with COPD
High CO2 levels and difficulty maintaining sats
The ventilatory center is in the _____ and works by monitoring _____
Brainstem
CO2
In COPD, airway obstruction is worse on (expiration/inspiration)
Expiration
I:E consideration for COPD
Increase expiration time. Remember that expiration time is passive (there is a limit to how fast you can expire).
Common s/s for someone with COPD
Dyspnea and wheezing
What is dyspnea?
The subjective sensation of not being able to get enough air. Often described as breathlessness, air hunger, SOB, labored breathing, and preoccupation with breathing.
Lung volume changes with COPD
Increased TLC, VC, FRC, and RV. Decreased TV and IC.
Basically, FRC is falsely increased because the lung tissue has lost it’s elasticity (less elastic recoil).
For someone with COPD, CO2 levels are usually worse at (day/night) because _____
Night. Because they are unconscious and unaware that they need to compensate by increasing their RR, etc.
Common obstructive disorders
Asthma, emphysema, chronic bronchitis
Patho of air trapping
People with COPD have mucus plugs on the bronchial walls. During inspiration, the airways are pulled open, allowing gas to flow past the obstruction. During expiration,decreased elastic recoil of the walls causes them to collapse onto the mucus and cause air trapping.
The trapped air in air trapping is useless volume because ventilation is not occurring. Air gets in, but is not coming out.
What is asthma?
A chronic inflammatory disorder of the airways associated with airway obstruction and bronchial hyperresponsiveness.
This airway obstruction is widespread but often reversible either spontaneously or with treatment.
Inflammation associated with asthma causes
1) Recurrent episodes of wheezing
2) Breathlessness
3) Chest tightness and cough (particularly at night and early in the morning)
4) Hyperresponsiveness to stimuli
What is atopy?
A genetic predisposition to developing an IgE-mediated hypersensitivity response to common allergens.
This is the strongest predisposing factor to the development of asthma.
What do we give asthmatics before surgery?
2 puffs of their inhaler and an anticholinergic
Patho of the asthmatic response to an allergen
1) The allergen binds to pre-formed IgE on a mast cell in the airway
2) The mast cell degranulate, releasing mediators such as histamine, leukotrienes, prostaglandins, etc. The effect is the opening of intercellular tight junctions
3) With cell junctions open, the antigen penetrates the junctions and activates submucosal mast cells.
4) Submucosal mast cells degranulate, causing bronchospasm, edema, and mucus secretion. The inflammatory response is initiated by chemotactic factors from mast cells.
5) In the late asthmatic response, epithelial cells are damaged due to products of eosinophils (which arrived as part of the inflammatory response)
Why is there V:Q mismatch in asthma?
Ait trapping and alveolar hyperinflation create areas of the lung that are being perfused but not ventilated
Risk factors for COPD
Cigarette smoking***** Passive smoking Air pollution Hyperresponsive airways Occupational factors Alpha1- antitrypsin gene mutation (results in early COPD development even in non-smokers)-rare-<1% of cases
Definition of chronic bronchitis
Hypersecretion of mucus and chronic productive cough that last for 3 months out of the year for at least 2 years.
Those with chronic bronchitis have mucus that is thicker than normal. Inspired irritants increase mucus production and increase the size and number of mucus glands.
This thick mucus makes it easier for bacteria to adhere as well. Repeated infections are common.
What are the acini?
Gas-exchanging airways
What is emphysema?
Destruction of the alveolar walls causes enlargement of the gas-exchange airways (mostly the alveoli) and decreased elastic recoil. There is no obvious fibrosis in this disease process.
Two types of emphysema
Centiacinar- damage and overinflation occurs in the respiratory bronchioles (middle of the acina)
Panacinar- Damage to the entire acina, but more focused on the alveoli (starts in the alveoli and will eventually progress to the bronchioles)
Patho of emphysema due to smoking
1) Toxins in smoke lead to endothelial damage, causing inflammation and infiltration of cells (neutrophils, macrophages, etc).
2) ROS and inflammatory cytokines inhibit antiproteases (alpha1-AT).
3) Imbalance between proteases and antiproteases causes breakdown of elastin in the alveolar septa. 4) Destruction septa and elastin reduces elastic recoil, which reduces the volume of air expelled during exhalation.
Function of alpha1 antitryspin
Inhibits a wide variety of proteases
What is atelectasis?
Collapse of lung tissue.
What is absorption atelectasis?
Result from the gradual absorption of air from obstructed or partially ventilated alveoli.
Obstructed makes sense.
Partially ventilated- pores of Kohn remain closed in shallow breaths. The alveolus becomes obstructed and can undergo absorption atelectasis. Can be restored with deep breathing– this is why incentive spirometry is important!
Absorption atelectasis can also occur with inhalation of concentrated O2 or anesthetics. This is compounded by shallow breathing from pain post-op.
What is bronchiectasis?
Persistent, abnormal dilation of the bronchi.
Usually due to chronic infections that begin in childhood (whooping cough, etc). These people are prone to having infections and experience chronic inflammation. Chronic inflammation leads to destruction of elastin and muscular components of the walls, leading to permanent dilation. This dilation can be cylindrical, saccular, or varicose.
What is restrictive lung disease?
Diseases that cause decreased compliance of the lung or chest wall.
Remember that compliance = (change in V) / change in P
This means that it takes more effort to expand the lungs on inspiration. People with these diseases tend to have rapid and shallow ventilation (increases dead space ventilation), and complain of dyspnea.
Most of the time, gas exchange is normal. In advanced disease, you will see decreased O2, increased CO2, pulmonary HTN, and cor pulmonale
Lung values that are decreased and remain the same in restrictive lung disease
Decreased:
- TLC
- FRC
- Reserve volume
- Vital capacity (nmL > 70mL/kg)
- FEV1
- FVC
- Total volume exhaled
Stays the same:
- Expiratory flow rates
- FEV1/FVC ratio (both values decrease, so the ratio remains the same)
FEV1/FVC ratio in COPD
Decreased due to reduction in FEV1
Classifications of RLD
1) Acute intrinsic (pulmonary edema)
2) Chronic intrinsic (diseased lung parenchyma)
3) Chronic extrinsic (chest wall problems, intra-abdominal (obesity), & NM diseases)
4) Diseases of the pleura and mediastinum
What is pulmonary edema?
Excess fluid in the interstitium and and alveoli of the lung.
Normally, the lung is kept dry by lymphatic drainage and surfactant (which repels water from entering the alveoli).
Two general causes of pulmonary edema
1) Increased capillary hydrostatic pressure (cardiogenic, hypertensive crisis, RV failure, etc)–Most common*
2) Increased capillary permeability (inflammatory process/ARDS)
Pulmonary edema due to increased capillary permeability
Will see high concentration of proteins and secretory products due to inflammatory process. Pulm edema associated with ARDS will result in diffuse alveolar damage
CXR findings of cardiogenic pulmonary edema
Butterfly patter or a perihilar distribution of opacities
What is ARDS?
Rapid form of respiratory failure often caused by diffuse pulmonary endothelial injury or sepsis. Causes massive pulmonary inflammation, which results in H20, solutes, and macromolecules diffusing from the intravascular space, into the lung parenchyma and alveoli.
Sepsis often co-exists, causing further injury due to inflammatory mediators.
Often times, ARDS signals the beginning of
Multiple organ system failure
What is MODS?
Multiple organ dysfunction syndrome. Often set off by ARDS. or sepsis Causes a hyper-dynamic, hyper-metabolic state similar to sepsis. Lungs are usually the first to fail. Followed by the liver, kidneys, GI tract (fails to act as a barrier and bacteria enter circulation) and the heart (V wall motion abnormalities).
If 3 organs are involved, mortality is often 100%.
What is aspiration pneumonitis?
Aspiration of acidic stomach contents causes inflammation, bronchospasm, damages the pulmonary capillary endothelium, and destroys surfactant producing cells. When surfactant production is disrupted, it results in stiff, conompliant lungs, and further edema into the alveoli.
Effect is similar to ARDS- pulmonary edema related to increased capillary permeability and atelectasis
Clinically, people with aspiration pneumonitis will demonstrate
1) Hypoxia
2) Tachypnea
3) Bronchospasm
4) Pulmonary vasoconstriction (can lead to pulm HTN)
5) CXR changes (won’t show up until 6-12 hours later and are usually in the RLL)
Treatment of aspiration pneumonitis
1) Intubate and ventilate**
2) High FiO2 and PEEP
3) Beta-2 agonist to treat bronchospasm
4) Fiberoptic bronchoscopy (if solid material)
5) Lavage with 5mL NS (controversial)
6) Antibx and steroids (controversial)
Cardiogenic pulm edema
LV failure causes backup into the lungs and increased cap hydrostatic pressure.
S/S related to SNS activation and edema
1) Extreme dyspnea and tachypnea (need to intubate)
2) HTN
3) Tachycardia
4) Diaphoresis
5) Sense of impending doom
Neurogenic pulm edema
Flash edema. Occurs minutes to hours after brain injury (especially when involving the medulla)
1) Massive SNS discharge in response to CNS insult
2) Generalized vasoconstriction causes increased hydroaststic pressure and transudation of fluid into the lungs
Very similar to cardiogenic form. Only difference really is the cause.
Treatment of neurogenic pulm edema
Decrease ICP
Increase FiO2, PEEP
Resolution occurs within a few days
Avoid diuretics because it won’t treat the cause
Illicit drugs that cause pulm edema
Heroin- causes high permeability (often due to smoking it)
Cocaine- pulmonary vasoconstriction and/or MI will result in pulm edema
Treatment is supportive
When does high altitude pulm edema occur
After 48-96 hours at 2500-5000m in altitude. Also by rapid ascent.
Treatment for high altitude pulm edema occur
O2, NO, descent
Re-expansion pulm edema
Occurs if a lung is deflated and then re-inflated due to evacuation of the pneumo or pleural effusion. More common if >1L of air/fluid in the pleural space, >24 hours of collapse, and if re-expansion occurs rapidly.
Overall, it enhances capillary membrane permeability. Treatment is supportive (don’t give diuretics).
