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).
Neg-Pressure Pulm Edema
Occurs within minutes to 2-3 hours after acute upper airway obstruction (in a spont-breathing patient). Caused by:
1) Post-extubation laryngospasm (may need to re-intubate and send to ICU)
2) OSA
3) Epiglottitis
4) Tumor
5) Obesity
6) Hiccups
Usually self-resolves within 24 hours.
Patho of Neg-Pressure Pulm Edema
High negative pressure causes:
1) Decreased INTERSTITIAL hydrostatic pressure
2) Increased venous return
3) Increased afterload on LV
4) Increased SNS outflow (HTN and central pooling)
All these factors together increase transcapilary gradients favoring edema. Also causes hypoxemia and associated SNS activation.
It is easy to confuse symptoms of Neg-Pressure Pulm Edema with
Aspiration or PE
S/S of Neg-Pressure Pulm Edema
Tachypnea, cough, sats below 95%
Treatment of Neg-Pressure Pulm Edema
Self limited. Maintain airway, give supplemental O2, PPV if necessary
Progressive fibrosis can cause
Puln HTN, cor pulmonale, pneumothorax, and dyspnea.
Is fibrosis reversible?
No
Why is R sided heart failure more difficult to treat than L?
Ionotropes don’t work on the right side of the heart because the left side receives the majority of SNS outflow.
What is a granuloma?
collection of immune cells known as macrophages. Granulomas form when the immune system attempts to wall off substances that it perceives as foreign but is unable to eliminate.
What is sarcoidosis
Systemic granulomatous disorder, often affecting the lungs and lymph nodes. The exact cause is unknown. The granulomas can occur anywhere (liver, spleen, optic and facial nerves) but the lungs are the worse because it causes difficulty breathing. Granuloma in the heart is rare, but can cause dysrhythmias and restrictive cardiomyopathy.
Resp effects of sarcoidosis
1) Pulm HTN and cor pulmonale are likely
2) Deceased diffusion ability of alveoli
3) Can affect the larynx in 1-5% of patients, and can interfere with the passing of the ETT
People with sarcoidosis often present to the hospital for
mediastinoscopy for diagnosis
People with sarcoidosis may have imbalances with this electrolyte
Calcium
Patients with sarcoidosis are often on __(med)___ and may need ____ before surgery
Chronic corticosteroids
Stress dose of steroids peri-operatively
Hypersensitivity pneumonitis
Diffuse interstitial granulomatous reaction in the lungs in response to inhalation of dust containing fungi, spores, and animal or vegetable material.
Dyspnea and cough begins 4-6 hours after exposure followed by leukocytosis and eosinophilia. Can develop fibrosis with repeated episodes.
May have decreased O2 d/t hyperventilation.
CXR shows multiple pulmonary infiltrates.
Eosinophilic Granuloma
Will commonly lead to pulmonary fibrosis. Treat with corticosteroids.
Pulmonary Alveolar Proteinosis
For some unknown cause, lipid-rich proteinaceous material is deposited into the alveoli.
Results in dyspnea and decreased O2.
Pulmonary Alveolar Proteinosis may be associated with these diseases
AIDS, chemo, or inhalation of mineral dust.
Treatment of Pulmonary Alveolar Proteinosis
May require whole-lung lavage with double-lumen tube to remove alveolar material and improve macrophage function. It can be challenging to maintain O2 sats during lavage.
Lymphangiomyomatosis
Proliferation of the smooth muscle in the abdominal and thoracic lymphatics, veins, and bronchioles. Results in combined restrictive and obstructive disease, with decreased diffusion capacity.
Clinical presentation of Lymphangiomyomatosis
Women of child-bearing age (may be related to steroid hormone metabolism)
Progressive dyspnea, hemoptysis, recurrent pneumothorax, and ascites.
Death usually occurs within 4 years.
Overview of EXTRINSIC restrictive lung disease
1) Lungs are compressed, resulting in increased WOB. There is a decrease in lung volume and increase in airway resistance.
2) Abnormal chest wall mechanic
- Thoracic deformity can cause RV dysfunction and chronic compression of pulmonary vasculature
- Cough may be impaired, leading to chronic infection and development of obstructive component
FRC is increased of decreased with obesity?
Decreased and there is V:Q mismatch (this is why we need to pre-oxygenate obese people a lot). Excessive weight on diaphragm/chest wall.
Kyphosis
A cause of external restrictive lung disease. Anterior flexion of vertebral column.
Spine angle and resp effects
60- dyspnea with exercise
100- Alveolar hypoventilation, decreased O2, erythrocytosis, pulm HTN and cor pulmonale
110- VC <45%, respiratory failure
In those with costovertebral abnormalities, be wary with these drugs
CNS depressants- increased risk of hypoventilation and pneumonia
Pectus excavatum
Inward concavity of sternum
Pectus carinatum
Outward projection of the sternum
If someone has flail chest, you have to do this until cage stabilization occurs
Intubate
Use this measurement to assess the extent of NM disease on ventilation
VC
Examples of NM disorders that may affect ventilation
1) Diaphragmatic paralysis
- Breathing in the supine position may resemble flail chest, as abdominal contents push the diaphragm into the chest
- Can be caused by neoplastic invasion of the phrenic nerve
- Infants may need plication (pacing) of the diaphragm
- Transient diaphragmatic paralysis may occur after abdominal sx d/t phrenic nerve irritation
- Will result in decreased TV, increased RR, and increased A-a gradient. Need IS to prevent atelectasis
2) Spinal cord transection at or below C4
- Causes loss of expiratory muscles. Makes expiration and coughing difficult.
- PSNS dominance may cause bronchoconstriction
3) Guillian-Barre
4) MG
5) Myasthenic syndrome
6) Muscular dystrophy
- Inspiratory muscle weakness, impaired cough, and aspiration risk (d/t impaired swallowing)
- Avoid CNS depressants
Pneumothorax is
Air in the pleural space. Air separates the visceral and parietal pleura, destroying the negative pressure that should exist in the pleural space. This disrupts the state of equilibrium that normal exists between the recoil forces of the lung and chest wall. No longer held in check by the recoil forces of the chest wall, the lung fulfills its tendency to recoil by collapsing towards the hilum.
Empyema is
an infected pleural effusion
Difference between transudative and exudative effusion
Transudative is due to systemic factors (sepsis)
Exudative is due to local factors
Idiopathic pneumothorax
Air in the pleural space due to a defect in the parietal or visceral pleura
Tension Pneumo
The site of rupture acts as a one-way valve. Air enters the pleural space during inspiration and is not able to leave during expiration. Common after rib fracture of barotrauma. Air compresses the already recoiled lung, causing compression atelectasis, and pushing against the mediastinum, compressing and displacing the heart and great vessels.
Must be decompressed immediately!! If chest tube not immediately available, insert a large-bore needle into the pleural space through the second anterior intercostal space to decompress it.
100% O2 also improves the rate of air resorption by 4x.
S/S of Pneumo
Acute dyspnea Ipsilateral chest pain Decreased O2, increased CO2 Hypotension and tachycardia Decreased chest wall movement Decreased or absent breath sounds Hyperresonant percussion
FEV1 tells you
the RATE at which you can expire during the 1st second of expiration
Pulmonary emboli commonly arise from
Deep veins of the thigh
Pulmonary HTN is defined as
PA pressure 5-10mmHg above normal
or
Just a PA pressure over 20mmHg
PA HTN is usually caused by endothelial dysfunction resulting in
Overproduction of vasoconstrictors (thromboxane and endothelin) and underproduction of vasodilators (prostacyclin and NO)
Cause of PA HTN
Usually idiopathic (may be environmental or genetic)
PA HTN associated with respiratory diseases is usually mild to moderate in severity
Lung cancers are also called
Bronchogenic carcinomas
Heavy smokers have a ___x greater risk of developing lung CA than non-smokers
20x
Smoking can also be associated with CA in these organs
Larynx, oral cavity, esophagus, and urinary bladder.
Three types of lung CA
1) Non-smal cell lung CA
- Squamous cell CA
- Adenocarcinoma
2) Large Cell carnimona
3) Small-cell carcinoma
Squamous cell CA
Slow growing, and located near the hilus and projects into the bronchioles. First presents with cough and hemoptysis (b/c located near large airway)
Adenocarcinoma
Moderate growth and mortality.
Growth is usually on the periphery of lung tissue.
Least correlated with smoking.
Large Cell CA
Rapid
Small Cell (oat cell) CA
VERY RAPID and high mortality (1% 5 year survival rate)
Most correlated with smoking.
Produces ectopic hormones.
TNM System
T- Size/direct extent of the primary tumor
N- Nodal involvement
M- Metastasis
Stage I
Tumors that are T1
Either no nodal involvement or has some nodal involvement in the ipsilateral hilar region
Stage I could also be T2 with no nodal involvement
Stage II
T2 with mets to the ipsilateral lymph nodes
Stage III
Any tumor with T>2
Any tumor with mets to the lymph nodes in the mediastinum or distant sites (commonly the brain or bones)
Squamous cell CA is the (most/least) common, and has the (best/worst) survival rate
Most common
Best survival rate
Does lung CA respond well to chemo?
No. Usually uses radiotherapy.
Examples of common mediastinal tumors
Thymomas, teratomas, lymphomas, retrosternal goiters.
Effect of mediastinal tumors
Airway obstruction, decreased lung volume, pulmonary artery compression, heart compression, SVC compression.
SVC syndrome
Compression of SVC by a tumor, causing dyspnea, dilation of collateral veins of face and neck, edema of face, neck, conjunctiva and upper chest. HA, and altered mental status.
Basically, venous congestion of the upper body.
Tx of pleural effusion
Thoracentesis
Pneumomediastinum
Air in the mediastinum. Can be caused by trach, alveolar rupture, cocaine use, or be idiopathic.
S/S of pneumomediastinum
Sudden increased WOB, cough, emesis, SQ emphysema in arms, abdomen, and neck. Can decompress into the pleural space and cause a pneumothorax.
Tx is O2 and supportive therapy. Occasionally need surgical decompression.
Bronchogenic cysts
Fluid or air-filled cysts from the primitive foregut that are lined by resp endothelium. Mass may be mediastinal or in the lung parenchyma.
Manifestations range from asymptomatic to recurrent infx to airway obstruction.
Hypothetical anesthetic risks include N2O expansion of cyst and ball-valve effect with PPV.
How dumb is patho?
So dumb.
Can negative pressure edema occur in someone who is being mechanically ventilated?
No, because they are ventilating using PPV.
Why do obese people have VQ mismatch?
Compression atelectasis
What happens if >60% of pulmonary circulation is occluded by a PE?
Sudden death, CV collapse, cor pulmonale
When does negative pulm pressure edema occur?
2-3 hours after acute upper airway obstruction in a spontaneously breathing patient
Thoracic deformities tend to cause
Compression on pulmonary vasculature and RV dysfunction
What is an idiopathic pneumothorax?
Pneumo caused by a defect in the parietal or visceral pleura
S/S of PE
Decrease in EtCO2 Decreased O2 Increased HR Systemic hypotension Decreased CO Shock Increased PA BP VQ imbalances Chest pain
Reaction of the lungs to a PE
Hypoxic vasoconstriction Decreased surfactant (less O2 supply to Type II cells) Pulm edema Atelectasis Release of inflammatory substances
