Pulmonary Disease Flashcards
Define tidal volume
Amount of air passing in and out with each breath
What are three different types of cells that you find in alveoli and what do they do?
Epithelial (Type I) - line in the inside of the alveoli and are thin enough to allow gas exchange (face air side)
Secretory (type II) - which secrete surfactant to break the surface tension of water when it enters the lungs through breathing
Macrophages - which phagocytize pathogens or particles for disposal
How does the body detect increased levels of CO2?
The arterial chemosensors are sensitive to levels of CO2 concentration and affect mostly the respiratory rate alone
Define Peak expiratory flow rate (PEFR) and why is it measured?
The maximum velocity of air on forced expiration - really important in asthma
What is FEV1
The volume of air that can forcibly be blown out in one second, after full inspiration
What is FCV
The volume of air that can forcibly be blown out after full inspiration
FEV1/FVC ratio - should be about 75-80% (this is most helpful in COPD)
When FEV1/FVC is decreased, this signifies an obstructive pattern
Asthma classifications and treatment of each
Intermittent:
–<2 asthma attacks per week, FEV1 >80%, Minimal use of rescue inhaler
—-Albuterol inhaler given PRN
Mild persistent:
–>2 asthma attacks/week, night time sxs, FEV1 >80%, >2 uses of rescue inhaler
—Albuterol inhaler PRN plus inhaled steroid daily (Flovent - fluticasone)
Moderate persistent:
–Daily asthma attacks, >1/week night time sxs, FEV1 60-80%, daily use of rescue inhaler
—- Albuterol PRN, inhaled steroid, plus leukotriene modulator (Singulair - montelukast)
Severe persistent:
–Continuous asthma sxs, frequent night time sxs, FEV1 <60%, frequent rescue inhaler use
—-All of the above plus systemic steroids like prednisone, either in tapers or low maintenance doses
Basic management of asthma exacerbation - stepwise progression
Albuterol nebs and/or atrovent - (duoneb) - helps treat bronchospasm and also dries up secretions
If this does not work, can give Solu-medrol (methylprednisolone) IV for really bad asthma exacerbation.
Heliox - oxygen mixed with helium. Helium can get into really tight airway spaces
Intubation for extreme cases
Most common risk factor for COPD
Cigarette smoking
What are the two types of COPD
Emphysema - abnormal and permanent enlargement of the alveoli, making them useless
—“Pink puffers” - pink complexion, barrel chested, increased respiratory rates, skinny, pursed lips, mild sputum that is clear
—–Bronchodilators, O2
Chronic bronchitis - chronic productive cough with significant airflow limitations with productive cough for 3 months in two consecutive years
—“Blue bloaters” - cyanosis, edema, loud wheezing and rhoncci, copious mucous production
—–Antibx, mucolytics/expectorants
Types of inhalers used in COPD
SABA - Short Acting Beta-Agonists - Albuterol (sold as ProAir)
SAMA - Short Acting Muscarinic-Agonists - Ipratopium (Atrovent)
—Combination of the two is Combivent MDI or DuoNeb solution
LABA - Long Acting Beta-Agonist - Salmeterol (Serevent)
LAMA - Long Acting Muscarinic-Agonist - tiotropium (Spiriva)
Inhaled glucocorticoids - Fluticasone (Flovent MDI), Budesonide (Pulmicort MDI)
—Combined LABA and glucocorticoids: Symbicort and Advair Diskus
What often causes COPD exacerbation
70-80% of exacerbations are caused by infection
Continued smoking and poor medication adherence are also causes
Mainstay of treatment for COPD
Albuterol Nebulizer
Can augment with Ipratopium to get DuoNeb
O2 given should be medical air to keep O2 above 88% but at lowest possible to reduce free radical production which could happen in hyper-oxygenation
Antibiotic choices in patients with COPD exacerbation
If infectious sxs are also present, consider antibxs.
Most frequent isolated bacteria from patients with COPD is S. pneumoniae
—-Therefore Doxycycline 100mg PO/IV BID is recommended
Also need to consider if there is a risk for Pseudomonas (frequent antibx courses, recent hospitalization, previous Pseudomonas infection, FEV1 <50%.
—-Then levofloxacin 750mg PO/IV
Define Bronchiectasis and what are it’s treatments
Classified as an obstructive lung disease
Permanent, abnormal dilation and destruction of bronchial walls, most often caused by recurrent inflammation or infection of the airways
Different from chronic bronchitis dominant COPD because alveolar are not necessarily affected but the airways are
About half of cases are caused by cystic fibrosis
CXR shows Tram Tracks
Antibiotic treatment should be tailored to previous cultures
Treatment of cystic fibrosis
Postural drainage
Inhaled recombinant human deoxyribonuclease (rhDNase) to cleave DNA from the mucus to make it less sticky
Inhaled hypertonic saline
Inhaled bronchodilators
If acute infection - given antibx that are tailored to past sputum cultures
What is Cor Pulmonale?
RV hypertrophy which results in less blood being able to enter the RV because it is so dilated.
Often caused by pulmonary hypertension
Symptoms of Pulmonary Hypertension
Cyanosis can be present - clubbing
JVD
A loud S2 (pulmonic valve closure)
Hepatojugular reflux
Parasternal heave
Anasarca - edema of the entire body
What measures pulmonary artery pressure?
Swan Ganz catheter
Enters through Superior Vena Cava down through the RA, into the RV, into the pulmonary artery
Treatment of pulmonary hypertension
Usually caused by emphysema which will never go away however the pulmonary hypertension can be treated:
High-dose calcium channel blockers (Nifedipine)
Phosphodiesterase-5 inhibitors (Viagra) result in pulmonary vasodilation
Prostaglandins (epoprostanol) however when given nebulized, half life is in seconds so it needs to be given in the hospital (Veletri)
—Most effective
Atrial Sepstostomy - surgical procedure where a hole is placed between RA and LA dramatically decreasing pressure in RA but now there is a lot of unoxygenated blood in circulatory system - could cause syncope
Lung and/or Heart Transplant
Virchow’s Triad for VTE
Alterations in blood flow: Immobilization, pregnancy, obesity
Factors in the vessel wall: Trauma, endothelial injury d/u sepsis, surgery, catheterization
Factors affecting the properties of the blood (procoagulant state): contraceptives, genetic thrombophilia, cancer, acquired thrombophilia
Scoring system to rule out PE
PERC Rules:
Age <50
HR <100
SpO2 >95%
No unilateral leg swelling
No hemoptysis
No recent trauma or surgery
No prior DVT or PE
No hormone use
If any positive, then the rule does not apply and qualifies to rule out by D-dimer
EKG findings in PE
S1Q3T3
S-wave in I
Q wave and inverted T wave in III
Gold Standard for diagnosing PE
Pulmonary Angiography - not always feasible, needs to be performed in the cath lab.
Ventilation-perfusion (VQ) scan should be performed in all clinically stable patients.
CT Angiography is very sensitive and specific so is often done first but not considered the gold standard. Patients must be able to tolerate IV contrast
Treatment of PE
Supplemental O2
IV fluids for those with hypotension
Low-molecular weight heparin should be first line
Unfractionated heparin should be used if GFR <40, if considerable risk for bleeding
Massive PE that is causing hypotension should receive fibrinolysis (tPA) or thrombectomy
Warfarin should be started with LMWH on the same day - target INR 2.5-3.5
Difference between transudative and exudative pleural effusions (basics, not labs)
Fluid is considered exudative (inflammatory) if
—Infected or inflammatory fluid moves into the pleural space from lung inflammation, impaired lymph drainage, cancer, transdiaphragmatic movement of inflammatory fluid from the peritoneum.
—Most common causes are malignancy, PE, infections, pancreatitis
Transudative effusion will usually be normal pleural fluid
—Associated with CHF - increased pulmonary venous pressure so plasma leaks into the alveolar and pleural space
Risk factors for developing pneumothorax
Primary spontaneous pneumothorax:
—Male, tall, slender, smoker, family history
Secondary spontaneous pneumothorax:
—Blebs that rupture in the lung, causing small tear in the pleura, leading to tension pneumothorax - Could happen in Emphysema COPD patients, or intubated patients with a bleb - Necrotizing PNA, lung cancer, Tb
Iatrogenic pneumothorax:
—Central line placement, transthoracic needle biopsy
Traumatic pneumothorax:
—Trauma
Tension Pneumothorax: What is it? Signs and symptoms and treatments
Most serious form of pneumothorax
Occurs when equilibrium is never reached within the pleural cavity and the pneumothorax continues to expand, putting pressure on all organs within the chest wall
Can be caused by any other cause of pneumothorax - just an equilibrium is not met
Symptoms include SOB, chest pain, JVD, a falling blood pressure, rising heart rate, hypoxia and a late sign is tracheal deviation away from the affected side.
Needs emergency decompression: Insert a 14g IV catheter into 2nd intercostal space at the mid clavicular line. The needle is withdrawn, leaving the catheter in place.
This allows decompression to allow the other lung to function while you await a chest tube placement for the affected lung.
Treatment of primary spontaneous pneumothorax
If the pneumothorax is <2cm then the pt can be discharged home with close follow up
If it is >2cm then can give Nitrogen Washout Maneuver
—Patient is put on non-rebreather and given 100% O2 for 12-24 hours to help nitrogen move from pleural space into the lung and then exhaled.
Treatment of secondary spontaneous pneumothorax
Aspiration to re-inflate the lung via chest tube is recommended for any secondary spontaneous pneumothorax >2cm
If purely air, then can use smaller chest tube (8Fr - 12Fr)
Tube is inserted anteriorly (in the 3rd ICS at the midclavicular line) or laterally (in the 5th ICS mid axillary line) and then attached to a closed-chest drainage system (Pleurevac)
Larger chest tube is required if there is a hemo/pneumothorax such as in trauma (24Fr - 32Fr)
Differences on CXR of viral vs bacterial PNA
Bacterial is usually limited to a lobar infiltrate
Viral is usually diffuse, hazy, multifocal
Peripheral ground glass opacities
Bacterial causes of PNA
50% of community acquired cases are Strep pneumoniae
30% are H. influenzae
What is HAP and how do you treatment it
PNA that occurs 48 hours after admission
Frequently caused by Staph aureus, strep pneumoniae, haemophilus influenzae
Need to get a sputum culture to appropriately tailor antibxs
Should usually treat broadly with gram negative and MRSA coverage
—MRSA - Linezolid or Vancomycin
—Should cover for Pseudomonas - Cefepime or Zosyn or Levofloxacin
If at high risk for mortality or IV antibx in the last 90 days:
Need two of the following plus MRSA coverage:
Zosyn
Cefepime
Levofloxacin or Ciprofloxacin
Imipenem or Meropenem
PLUS Vanc or Linezolid
What are the testing methods used to rule out Tuberculosis
Primary screening method for Tb infection (active or latent) is the PPD - not diagnostic
—Cutoff of 5mm or more of induration - patients that are HIV+, have abnormal CXR, significant immunosuppression, people who have had recent contact with people with Tb
—Cutoff of 10mm or more induration - Patients with IVDU, residents of nursing homes, prisoners, homeless, minority groups, healthcare workers
—Cutoff of 15mm or more - Young and healthy people, general population
Acid-fast bacilli - most sensitive - Need 2 smears to exclude it
Newer testing (QuantiFERON Gold and T-spot Tb) offer ELISA assay for rapid results while awaiting acid-fast bacilli test
Any positive test should trigger a test for HIV
***Definitive diagnosis by culture of M. tuberculosis x3
Treatment for Tuberculosis
4 drug therapy - RIPE:
Rifampin
Isoniazid
Pyrazinamide
Ethambutol
Therapy continues for 6 months - 9 months with HIV
If latent Tb - can just treat with isoniazid for 9 months
If a patient is on a ventilator and begins to have respiratory failure and is becoming more hypoxic what do you do?
Remove patient from the ventilator and hand ventilate with Ambu-bag
Stepwise Treatment of a patient about to arrest from respiratory failure
Call a code
Assist into a more upright position
Suction airway to make sure there is nothing obstructing
Apply O2 - if needed, take off vent and oxygenate manually
Reassure the patient to reduce anxiety
Consider administration of bronchodilator
Insert an IV
Only after these steps have been accomplished can you safely proceed to diagnostics
Treatment of Respiratory Failure
For mild cases, can administer oxygen and bronchodilators while beginning to treat the underlying cause (PNA)
In moderate respiratory failure caused by obstructive pattern, can give non-invasive positive pressure ventilation (CPAP, BiPAP)
—-Must not be very hypoxic or acidotic because they could progress to AMS
If severe respiratory failure, will need endotracheal intubation with mechanical ventilation
Two types of non-invasive positive pressure ventilation
CPAP - Continuous positive airway pressure
—Delivers a constant flow of gas at high pressures
—-Will not cycle with regard to respirations
—Provides the equivalent of PEEP (positive end-expiratory pressure)
—Works well for asthma, sometimes COPD
BiPAP - Bilevel positive airway pressure
—Cycles in regard to respiration, that is, the device detects when the patient initiates a breath and cycles to another pressure during the inspiratory phase and then when the breath is over, will revert to a lower pressure
——Makes taking a breath easier
—Great for COPD exacerbations, CHF, not as great for asthma
Intubation sequence
Sedation: Etomidate, propofol
Paralysis: Succinylcholine, Rocuronium
Pre-oxygenation by bag-valve mask
Visualization of the vocal cords by direct laryngoscopy or by video larynoscope
Passing the endotracheal tube (supported by stylet) through the vocal cords
Remove the stylet carefully and then inflate the cuff at the end of the tube
Confirm placement by colorimetric capnography, auscultation of the breath sounds with no gastric gargling, observation of bilateral chest excursion, CXR to assess tube depth
Securement of the ETT to the face
Then keep on sedative drip so they do not wake up
How would an ABG appear in acute respiratory distress syndrome (ARDS)
Shows rapid decrease in pH <7.2
Decreased PaO2:FiO2 ratio
Mild ARDS - Ratio is 201-300mmHg
Moderate ARDS - Ratio is 101-200mm Hg
Severe ARDS - Ratio is <100mm Hg
Phases of ARDS
Acute Phase
–Breakdown of the Type I epithelial (alveolar)/endothelial (capillary) barrier due to inflammatory stress causing flooding of the alveoli with protein-rich fluid
—Dysfunction of Type II cells so that surfactant production is impaired
—Alveolar collapse then occurs, leading to impaired gas exchange and increased dead space
——-This causes pulmonary HTN
—This itself causes inflammation, causing a chain reaction to spread
Proliferative Phase
—With mechanical ventilation there is clearance of alveolar fluid
—Soluble proteins are removed by diffusion between alveolar epithelial cells
—Type II cells begin to differentiate into Type I cells and re-epithelialize denuded alveolar epithelium
—Further epithelialization leads to increased alveolar clearance
Recovery Phase
—Gradual resolution of hypoxemia
—Improved lung compliance
—Infiltrates disappear
—PFTs improve, often normalize
Fibrotic Phase
—Some people will develop increased fibrin from the amount of damage to the normal lung architecture
—Alveolar space is filled with mesenchymal cells and their products
—Re-epithelialization and new blood vessel formation occurs in disorganized way
—Increased thickening of intersititum due to fibrin which causes decreased lung compliance
—Fibrosing alveolitis and cyst formation
Normal VBG
pH 7.35 - 7.45
PaO2 >90 75-89 - mild hypoxia <75 severe hypoxia
PaCO2 35 - 45
HCO3 18-24
Peak inspiration pressure (PIP): What is it and what is a normal range?
Maximum pressure during inspiration
Should be less than 35
Plateau Pressure: What is it and what is the range?
Measure at end of inspiration with hold
Measures lung compliance
Should be less than 30
What is pulses paradoxus
Changes in intrathoracic pressure that causes a drop in blood pressure during inspiration.
Occurs often in asthma however can also occur in cardiac tamponade and sometimes in pericarditis
Is asthma obstructive or restrictive?
Obstructive
Cannot get air out - you will have hyper-resonance because of air trapping
What are the laboratory and diagnostics in COPD
Low flattened diaphragm on CXR
FEV1 and all other measurements of expiratory airflow reduced (obstructive)
Total lung capacity, functional residual capacity and residual volume are increased
What do you do if you have someone with a positive PPD and a CXR negative for Tb
Offer them 6 months of isoniazid (INH)
Could have Tb but it has just not shown on the CXR yet
What type of pressure room is used for Tb
Negative pressure room
What is the baseline evaluation needed before starting treatment for Tb
Need LFTs weekly because medication regimen for Tb is very hepatotoxic
CBC, BMP
If the pt is taking Ethambutol - need visual acuity testing and red-green color perception
What is the treatment for outpatient CAP?
Low severity?
Moderate to High severity?
Low severity: Healthy, no use of antibx within the last 3 months, no comorbidities or risk factors for MRSA or pseudomonas:
Amoxicillin 1g TID
or
Doxycycline 100mg BID
or
Macrolide (Azithromycin or clarithromycin)
Moderate to High Severity:
Treating for MDR S. Pneumoniae
-Respiratory fluoroquinolone (Levofloxacin or Moxifloxacin) - monotherapy
or
[Augmentin or cefpodoxime] + [Macrolide or doxycycline)
What is the inpatient management of CAP?
Nonsevere?
Severe (ICU)?
Nonsevere:
Monotherapy with respiratory fluoroquinolone (Levofloxacin or moxifloxacin)
or
Beta lactam (ceftriaxone) + macrolide (azithromycin)
Severe - ICU:
Ceftriaxone + (IV fluoroquinolone or IV Azithromycin)
or
If Pseudomonas. aeruginosa suspected - Zosyn or meropenum or cefepime + Azithromycin
or
If MRSA is suspected: Above + Vancomycin or linezolid
Treatment of VAP
Pseudomonas is most common causative organism
Want MRSA coverage and double pseudomonal coverage
MRSA Coverage: Vanc or Linezolid
Gram negative with antipseudomonal activity: Beta-lactams based:
Zosyn
Cefepime
Imipenem or Meropenem
Gram negative with antipseudomonal activity:
Non-beta lactam based:
Levofloxacin or Ciprofloxacin
Genamicin or Tobramycin
What is Sarcoidosis and what is the clinical presentation and diagnostics
What is the mainstay of therapy?
Sarcoidosis: Disease of unknown etiology characterized by interstitial lung disease and non-caseating granulomas
Most often affects the lungs and lymph nodes in the chest.
Symptoms:
Progressive dyspnea
Nonproductive cough
Rales (Velcro crackles) may be noted
Diagnostics:
CXR for staging
PFTs
Bronchoscopy with transbronchial biopsy of lung parenchyma for dx
Mainstay of therapy is steroids
Laboratory studies for patients in ARDS
Refractory hypoxemia is a hallmark feature
CXR may be “whited out” or have diffuse bilateral infiltrates
How will pulmonary function tests look in patients with restrictive lung disease?
What are some examples of restrictive lung disease
Total lung capacity will be reduced
Functional residual capacity will be reduced
Residual volume will be reduced
Examples of restrictive lung disease:
-Morbid obesity
-Sarcoidosis
-Pulmonary fibrosis
Plural effusions: Exudative vs transudative (lab values)
Exudative:
—Ratio of pleural fluid protein to serum protein greater than 0.5
—Ratio of pleural fluid LDH to serum LDH greater than 0.6
—Pleural fluid LDH greater than two thirds of the upper limits of normal
Transudative:
—a pH of 7.60-7.64
—Protein content of less than 2%
—Few than 1000 white blood cells per cubic millimeter
—Glucose content similar to that of plasma
—LDH less than 50% of plasma
