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Acute Care NP Exam > Pulmonary Disease > Flashcards

Pulmonary Disease Flashcards

1
Q

Define tidal volume

A

Amount of air passing in and out with each breath

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2
Q

What are three different types of cells that you find in alveoli and what do they do?

A

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

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3
Q

How does the body detect increased levels of CO2?

A

The arterial chemosensors are sensitive to levels of CO2 concentration and affect mostly the respiratory rate alone

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4
Q

Define Peak expiratory flow rate (PEFR) and why is it measured?

A

The maximum velocity of air on forced expiration - really important in asthma

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5
Q

What is FEV1

A

The volume of air that can forcibly be blown out in one second, after full inspiration

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6
Q

What is FCV

A

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

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7
Q

Asthma classifications and treatment of each

A

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

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8
Q

Basic management of asthma exacerbation - stepwise progression

A

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

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9
Q

Most common risk factor for COPD

A

Cigarette smoking

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10
Q

What are the two types of COPD

A

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

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11
Q

Types of inhalers used in COPD

A

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

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12
Q

What often causes COPD exacerbation

A

70-80% of exacerbations are caused by infection

Continued smoking and poor medication adherence are also causes

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13
Q

Mainstay of treatment for COPD

A

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

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14
Q

Antibiotic choices in patients with COPD exacerbation

A

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

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15
Q

Define Bronchiectasis and what are it’s treatments

A

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

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16
Q

Treatment of cystic fibrosis

A

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

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17
Q

What is Cor Pulmonale?

A

RV hypertrophy which results in less blood being able to enter the RV because it is so dilated.

Often caused by pulmonary hypertension

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18
Q

Symptoms of Pulmonary Hypertension

A

Cyanosis can be present - clubbing
JVD
A loud S2 (pulmonic valve closure)
Hepatojugular reflux
Parasternal heave
Anasarca - edema of the entire body

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19
Q

What measures pulmonary artery pressure?

A

Swan Ganz catheter
Enters through Superior Vena Cava down through the RA, into the RV, into the pulmonary artery

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20
Q

Treatment of pulmonary hypertension

A

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

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21
Q

Virchow’s Triad for VTE

A

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

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22
Q

Scoring system to rule out PE

A

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

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23
Q

EKG findings in PE

A

S1Q3T3

S-wave in I

Q wave and inverted T wave in III

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24
Q

Gold Standard for diagnosing PE

A

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

25
Q

Treatment of PE

A

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

26
Q

Difference between transudative and exudative pleural effusions (basics, not labs)

A

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

27
Q

Risk factors for developing pneumothorax

A

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

28
Q

Tension Pneumothorax: What is it? Signs and symptoms and treatments

A

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.

29
Q

Treatment of primary spontaneous pneumothorax

A

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.

30
Q

Treatment of secondary spontaneous pneumothorax

A

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)

31
Q

Differences on CXR of viral vs bacterial PNA

A

Bacterial is usually limited to a lobar infiltrate

Viral is usually diffuse, hazy, multifocal
Peripheral ground glass opacities

32
Q

Bacterial causes of PNA

A

50% of community acquired cases are Strep pneumoniae
30% are H. influenzae

33
Q

What is HAP and how do you treatment it

A

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

34
Q

What are the testing methods used to rule out Tuberculosis

A

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

35
Q

Treatment for Tuberculosis

A

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

36
Q

If a patient is on a ventilator and begins to have respiratory failure and is becoming more hypoxic what do you do?

A

Remove patient from the ventilator and hand ventilate with Ambu-bag

37
Q

Stepwise Treatment of a patient about to arrest from respiratory failure

A

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

38
Q

Treatment of Respiratory Failure

A

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

39
Q

Two types of non-invasive positive pressure ventilation

A

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

40
Q

Intubation sequence

A

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

41
Q

How would an ABG appear in acute respiratory distress syndrome (ARDS)

A

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

42
Q

Phases of ARDS

A

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

43
Q

Normal VBG

A

pH 7.35 - 7.45
PaO2 >90 75-89 - mild hypoxia <75 severe hypoxia
PaCO2 35 - 45
HCO3 18-24

44
Q

Peak inspiration pressure (PIP): What is it and what is a normal range?

A

Maximum pressure during inspiration

Should be less than 35

45
Q

Plateau Pressure: What is it and what is the range?

A

Measure at end of inspiration with hold
Measures lung compliance
Should be less than 30

46
Q

What is pulses paradoxus

A

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

47
Q

Is asthma obstructive or restrictive?

A

Obstructive
Cannot get air out - you will have hyper-resonance because of air trapping

48
Q

What are the laboratory and diagnostics in COPD

A

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

49
Q

What do you do if you have someone with a positive PPD and a CXR negative for Tb

A

Offer them 6 months of isoniazid (INH)

Could have Tb but it has just not shown on the CXR yet

50
Q

What type of pressure room is used for Tb

A

Negative pressure room

51
Q

What is the baseline evaluation needed before starting treatment for Tb

A

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

52
Q

What is the treatment for outpatient CAP?
Low severity?
Moderate to High severity?

A

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)

53
Q

What is the inpatient management of CAP?
Nonsevere?
Severe (ICU)?

A

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

54
Q

Treatment of VAP

A

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

55
Q

What is Sarcoidosis and what is the clinical presentation and diagnostics
What is the mainstay of therapy?

A

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

56
Q

Laboratory studies for patients in ARDS

A

Refractory hypoxemia is a hallmark feature
CXR may be “whited out” or have diffuse bilateral infiltrates

57
Q

How will pulmonary function tests look in patients with restrictive lung disease?
What are some examples of restrictive lung disease

A

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

58
Q

Plural effusions: Exudative vs transudative (lab values)

A

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

Acute Care NP Exam (22 decks)

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