Pulm Flashcards

1
Q

What is alveolar hypoventilation?

A

Low PaO2, high PaCO2 (respiratory acidosis)
Etiology: pulmonary/thoracic diseases (COPD, OSA, obesity hypoventilation, scoliosis), neuromuscular diseases (MG, Lambert Eaton, Guillain Barre), drug-induced hypoventilation (anesthetics, narcotics, sedatives), primary CNS dysfunction (brainstem lesion, infection, stroke)
Normal Aa gradient (normal is less than 15)

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2
Q

What is VQ mismatch?

A

Etiology: atelectasis, pleural effusion, pulmonary edema, pulmonary embolism
Low PaCO2 (respiratory alkalosis) due to compensatory tachypnea
Elevated Aa gradient

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3
Q

What is delayed emergency from anesthesia?

A

Failure to return to consciousness w/in expected window of last administration of an anesthetic or adjuvant agent (typically 30-60m)
Etiology: drug effect, metabolic disorder, neurologic disorder
Presentation: respiratory failure (low pH, elevated pCO2, low pO2), bradypnea, bradycardia
Tx: ventilatory support

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4
Q

What is aspiration pneumonia?

A

Delayed in onset
Pathophys: lung parenchyma infection, aspiration of upper airway or stomach microbes (anaerobes) that colonize oropharyngeal secretions
Presentation: present days after aspiration event, fever, cough, foul-smelling/increased sputum, can progress to abscess; concurrent periodontal disease
CXR: infiltrate in dependent lung segment (classically RLL)
Mgmt: abx (clinda or beta lactam and beta lactamase inhibitor)

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5
Q

What is aspiration pneumonitis?

A

More acute in onset
An acute lung injury due to aspiration of acidic and sterile stomach contents.
Pathophys: lung parenchyma inflammation, aspiration of gastric acid with direct tissue injury
Presentation: present hours after aspiration event, range from no sxs to non-productive cough, decreased O2, respiratory distress
CXR: infiltrates (one or both lower lobes) resolve w/o abx
Tx: supportive (no abx)

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6
Q

What is atelectasis?

A

Lobar or segmental collapse of the lung that causes decreased lung volume
Etiology: due to mucus plugging
Pathophys: airway obstruction creates distal air trapping in alveoli, trapped air diffuses into blood stream, b/c no additional air can enter obstructed airway the alveoli become devoid of matter and collapse; to occupy vacated space, mediastinal structures are pulled TOWARD atelectasis
Common postop complication - results from shallow breathing and weak cough due to pain; common on POD2-3 following abdominal or thoracoabdominal surgery
Presentation: dyspnea, tachypnea, tachycardia
Lung exam: dullness to percussion and absence of breath sounds
CXR: opacification, w/ mediastinal shifting toward side of opacification, rib space narrowing
Tx: chest physiotherapy to prevent mucus plug (small), bronchoscopy to remove mucus plug (large); incentive spirometry for postop cases

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7
Q

What is post-operative atelectasis?

A

Impaired cough and shallow breathing
Due to airway obstruction from retained airway secretion, decreased lung compliance, postoperative pain, and medications that interfere with deep breathing
Present on POD2-3 from abd/thoracoabd surgery
high pH, low pO2, low pCO2
Tx: IS

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8
Q

What are postoperative pulmonary complications?

A

Complications: atelectasis, infection (pneumonia), bronchospasm, exacerbation of chronic lung disease, prolonged mechanical ventilation
RF: age >50, emergency surgery or surgery duration >3h, HF, COPD, poor general health
Preop strategies to reduce risk: smoking cessation at least 8w prior to surgery, sx ctrl of COPD (eg preop glucocorticoids if not well controlled), tx of any respiratory infections prior to surgery, pt education for lung expansion maneuvers (eg chest physical therapy, coughing, deep breathing exercises, incentive spirometry)
Postop strategies: incentive spirometry, deep breathing exercises, epidural analgesia instead of parenteral opioids, continuous airway pressure

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9
Q

What is a diaphragmatic hernia?

A

More common on L side b/c the R side tends to be protected by the liver.
Presentation: respiratory distress, deviation of mediastinal contents to opposite side
CXR: elevation of hemidiaphragm on CXR, nasogastric tube in pulmonary cavity*

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10
Q

What is a bronchogenic cyst?

A

Benign
Usually found in the middle mediastinum
Dx: CT scan

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11
Q

What is a thymoma?

A

Common in young male or female, 20% have myasthenia gravis, also assoc. with pemphigus
Usually found in the anterior mediastinum
Presentation: chest heaviness or discomfort; hoarseness, Horner’s syndrome, and facial and upper extremity edema may occur when tumors invade locally

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12
Q

What is a neurogenic tumor?

A

Located in the posterior mediastinum
Includes: meningocele, enteric cysts, lymphomas, diaphragmatic hernias, esophageal tumors, aortic aneurysms
Dx: MRI

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13
Q

What is a complicated parapneumonic effusion/empyema?

A

Caused by bacterial invasion of pleural space
Pleural fluid - exudative: low pH <7.2, low glucose <60, high protein, WBC >50k,
Pleural fluid gram stain and culture: positive
CXR: loculation (walled-off pleural fluid)
Tx: abx + drainage (chest tube)

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14
Q

What is an uncomplicated parapneumonic effusion?

A

Etiology: sterile exudate in pleural space
Pleural fluid: high pH >7.2, high glucose >60, WBC <50k
Pleural fluid gram stain and culture: negative
Tx: abx

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15
Q

What is spontaneous pneumothorax?

A

Assoc. features: primary - no preceding event or lung disease; Marfan, smoking, thoracic endometriosis, tall thin young men; secondary - underlying lung disease (eg COPD, cystic fibrosis; rupture of alveolar blebs is common)
Signs and sxs: chest pain, dyspnea, decreased breath sounds, decreased chest movement, ipsilateral hyperresonance to percussion
Dx: CXR
Imaging: absent lung marking, visceral pleural line
Mgmt: small (<2cm) - obs and supplemental O2 which enhances speed of resorption;
larger and stable - needle aspiration (2nd or 3rd ICS in midclavicular line or 5th ICS in mid or anterior axillary line)
hemodynamically unstable- chest tube/tube thoracostomy

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16
Q

What is tension pneumothorax?

A

Complication of subclavian central venous catheter placement
Assoc. features: life-threatening, often due to trauma or mechanical ventilation; rapid-onset dyspnea, tachycardia, tachypnea, hypotension, and distension of neck veins
Signs and sxs: same as spontaneous w/ HD instability, tracheal deviation away from affected side
High intrathoracic pressure compresses vena cava and impedes cardiac venous return resulting in decreased CO and hypotension
Imaging: same as spontaneous w/ contralateral mediastinal shift, ipsilateral hemi-diaphragm flattening
Mgmt: urgent needle decompression (needle thoracostomy) to prevent cardiovascular collapse followed by chest tube placement (tube thoracostomy) for definitive pneumothorax management

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17
Q

What is a pulmonary contusion?

A

Results in intra-alveolar hemorrhage and edema, complicates 35% of cases of blunt thoracic trauma
Clinical features: present <24h after blunt thoracic trauma; tachypnea, tachycardia, hypoxia
Dx: rales or decreased breath sounds, CT scan (most sensitive) or CXR w/ patchy, diffuse alveolar infiltrate not restricted by anatomical borders
Mgmt: pain control, pulmonary hygiene (eg nebulizer treatment, chest PT, supplemental O2 and ventilatory support

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18
Q

What is a massive PE?

A

PE complicated by hypotension and/or acute right heart strain.
[acute RH strain: JVD, R BBB]
Presentation: dyspnea, pleuritic chest pain, syncope, JVD, right bundle branch block
Dx: CT pulmonary angiography
Tx: respiratory and HD support, fibrinolysis (if no surgery w/in 10 preceding days)

An acute massive PE can cause abrupt increases in RA pressure to >10 and PA pressure >40. This can lead to decreased venous return to the LA, decreased CO, hypotension, and obstructive shock.

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19
Q

What is flail chest?

A

Pathophys: greater than/= 3 contiguous ribs fractured in greater than/= 2 locations –> flail chest segment
Findings: paradoxical chest wall motion w/ respiration, chest pain, tachypnea, rapid shallow breaths
CXR: rib fractures +/- contusion/hemothorax
Mgmt: pain control for uncomplicated rib fracture, supplemental O2, positive pressure ventilation (+/- chest tube) for flail chest/if respiratory failure

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20
Q

What is septic shock?

A

Presentation: fever, tachycardia, hypotension, poor urine output
Mgmt: securing airway, restoring adequate tissue perfusion through IV 0.9% saline (crystalloid) prior to administration of vasopressors, identifying underlying infection
Crystalloid should be given as IV boluses (500-1000ml) to improve SBP >90

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21
Q

What is a thermal burn?

A

Thermal injury to upper airway = burns on face, singeing of eyebrows, oropharyngeal inflammation/blistering, oropharyngeal carbon deposits, carbonaceous sputum, stridor, carboxyhemoglobin level >10%, history of confinement in a burning building
Presence of greater than/= 1 of these indicators warrants early intubation to prevent upper airway obstruction by edema

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22
Q

What is tracheobronchial rupture?

A

Secondary to blunt thoracic trauma
R main bronchus is most commonly injured
Presentation: pneumomediastinum and subcutaneous emphysema (palpable creptius below the skin)
XR: persistent pneumothorax despite chest tube placement and pneumomediastinum
Dx: high resolution CT scan, bronchoscopy, or surgical exploration
Tx: operative repair

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23
Q

What is asthma exacerbated respiratory disease?

A

Non-IgE mediated reaction resulting from aspirin-induded prostaglandin/leukotriene misbalance; increased production of pro-inflammatory leukotrienes
Seen in pts with hx of asthma or chronic rhinosinusitis w/ nasal polyposis
Presentation: bronchospasms (cough, wheezing, chest tightness), nasal congestion following aspirin ingestion (30m to 3h later)
Tx: avoidance of NSAIDS, aspirin, desensitization if NSAIDS are required, use of leukotriene receptor antagonists (eg montelukast)

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24
Q

What is hypertrophic osteoarthropathy?

A

Presentation: clubbing, sudden onset joint arthropathy, and periostosis of long bones, and synovial joint effusions
Assoc. w/ lung cancer
Dx: CXR to r/o malignancy and/or other lung pathology

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25
Q

What is respiratory distress syndrome?

A

Caused by immature lungs and surfactant deficiency
Inversely proportional to gestational age
RF: prematurity, maternal DM
Maternal hyperglycemia causes fetal hyperglycemia, which triggers fetal hyperinsulinism, which antagonizes cortisol and blocks maturation of sphingomyelin, a vital component of surfactant
Presentation: tachypnea, retractions, grunting, nasal flaring, and cyanosis at birth
XR: diffuse reticulogranular pattern (ground glass opacities), air bronchograms
Tx: corticosteroids, postnatal exogenous surfactant

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26
Q

What is clubbing?

A

Common causes: lung malignancies, CF, and R to L cardiac shunts
Due to entrapped megakaryocytes releasing PDGF and VEGF in distal fingertips

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27
Q

What is a bronchoscopy?

A

Initial procedure of choice in patients w/ hemoptysis (>600ml/24h or >100ml/h)
It can localize the bleeding site, provide suctioning ability to improve visualization, and include therapeutic interventions (eg balloon tamponade, electrocautery)

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28
Q

Asbestos

A

Asbestos exposure increases the risk of pulmonary fibrosis and malignancy.
Bronochogenic carcinoma is the most common malignancy diagnosed in pts exposed to asbestos.
Smoking acts synergistically w/ asbestos to further increase risk of lung cancer.

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29
Q

Pulmonary arterial hypertension.

A

LV systolic or diastolic dysfunction is a common cause of pulmonary HTN.
Tx: loop diuretics and ACE-i or ARBs.

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30
Q

Advanced dementia.

A

Leads to impaired swallowing and cough reflex.

Increased susceptibility to aspiration pneumonia.

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31
Q

What is an esophageal leiomyoma?

A

Located in the posterior mediastinum.
They are submucosal and usually asymptomatic.
They only produce symptoms when >5cm. Only large tumors should be removed.

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32
Q

Appearance of thymus on XR.

A

“Sail sign.”

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33
Q

Asthma + impending respiratory collapse.

A

Usually results in respiratory alkalosis (low CO2) due to hyperventilation.
Normal CO is bad = inability to maintain adequate ventilation, which is caused by respiratory muscle fatigue or severe air trapping and suggests impending respiratory collapse.

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34
Q

Treatment for community aquired pneumonia.

A

Presents w/ dyspnea, pleuritic chest pain, fever, productive cough
Focal increased breath sounds, crackles
Consolidative alveolar filling process on CXR
Dx of CAP requires presence of a lobar, interstitial, or cavitary infiltrate on CXR for confirmation. Clinical and physical findings are poor at predicting presence of pneumonia.
Sputum and blood cultures are typically NOT required in the OP setting as empiric oral abx are almost always curative.

Fluoroquinolone (eg moxi) or a beta lactam + macrolide (ceftriaxone + azithro)
Meds cover most common bacterial CAP organisms: s. pneumo, h. flu, legionella, and mycoplasma pneumoniae
Macrolide or doxycycline is needed to cover for atypical bacterial pathogens.

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35
Q

Criteria for long-term supplemental O2 therapy in COPD

A

Prolongs survival
Criteria for initiating LOT
1. resting PaO2 <=55 or pulse Ox <=88%
2. pulse Ox<=89% in pts w/ cor pulmonale, evidence of RH failure, or hematocrit >55%

36
Q

What is acute respiratory distress syndrome (ARDS)?

A

Inflammatory condition assoc. w/ infections, trauma, or other conditions (massive transfusion, pancreatitis) leading to capillary leakage and diffuse pulmonary edema
Presentation: fever, respiratory distress, hypoxemia, bilateral opacities
Lung injury causes release of proteins, inflammatory cytokines, and neutrophils into the alveolar space which leads to leakage of bloody and proteinaceous fluid into the alveoli, alveolar collapse due to loss of surfactant and diffuse alveolar damage which results in alveolar collapse and impaired gas exchange due to physiologic shunting and increased physiologic dead space
V=0, resulting in extreme V/Q mismatch, causing hypoxemia
Increasing FiO2 does not correct the hypoxemia b/c diffuse pulmonary edema prevents air from reaching alveoli throughout much of the lungs.
A-a gradient is increased
PaO2/FiO2 is decreased (<300)
Pulmonary edema leads to fluid collection w/in lung intersitium resulting in stiffening of the lungs (decreased lung compliance - due to both loss of surfactant and increased elastic recoil of edematous lungs)
Pulmonary arterial pressure is increased (pulm HTN) due to hypoxic vasoconstriction, destruction of lung parenchyma, and compression of vascular structures from positive airway pressure in mechanically ventilated pts
Pulmonary capillary wedge pressure (surrogate measure for L atrial pressure; helpful in diagnosing volume overload) is normal

37
Q

How to improve oxygenation

A

Increase fraction of inspired O2 (FiO2) or

Positive end expiratory pressure (PEEP) provided by the mechanical ventilator

38
Q

What is PEEP (positive end expiratory pressure)?

A

Prevents alveolar collapse during respiratory cycles, may reopen alveoli that have already collapsed, reducing shunting
High PEEP approaches may improve mortality in pts w/ severe ARDS

39
Q

What is FiO2?

A

Usually weaned to <60% as quickly as possible b/c prolonged high FiO2 increases the risk of pulmonary O2 toxicity (radical formation)
In pts requiring high levels of FiO2, PEEP levels should be increased (as long as a normal plateau pressure can be maintained (to reduce the risk of barotrauma)) to allow for reduction in the FiO2 as oxygenation improves.
[If high levels >60% required to maintain oxygenation, PEEP levels should be increased to allow for reductions in the FiO2 as oxygenation improves]

40
Q

Granulomatosis w/ polyangititis (GPA)

A

Lower respiratory tract involvement may lead to tracheal narrowing w/ ulceration - highly characteristic of GPA
CXR: multiple lung nodules w/ cavitation accompanied by alveolar opacities
Pts typically have anemia of chronic disease
Renal involvemnt is common: necrotizing crescentic pauci-immune glomerulonephritis
Dx: antineutrophil cytoplasmic antibodies; tissue biopsy is definitive (granulomatous inflammation)
Tx: high dose corticosteroids + cyclophosphamide or rituximab

41
Q

What is sarcoidosis?

A

Noncaseating granulomatous inflammation
Most commonly affecting the lungs
Characterized by bilateral hilar adenopathy on CXR
Renal involvement: interstitial nephritis or nephrolithiasis

42
Q

Asthma + GERD

A

Comorbid GERD is common in pts w/ asthma and can exacerbate sxs through microaspiration of gastric contents leading to an increase in vagal tone and bronchial reactivity
Presentation: sore throat, morning hoarsenes, worsening cough only at night, increased need for inhaler after meals
Obesity increases risk of developing GERD
Tx: PPI improves asthma sxs and peak expiratory flow rate in asthma pts w/ evidence of comorbid GERD

43
Q

What is aspirin-exacerbated respiratory disease?

A

Occurs in pts w. asthma and chronic rhinosinusitis
Presentation: sudden worsening of asthma and nasal congestion 30min to 3h after ingestion of nonsteroidal anti-inflammatories

44
Q

Aspergillosis

A

A subset of immunocompetent pts w/ hx of pulmonary disease (cavitary tuberculosis, sarcoidosis, bronchial cysts, neoplasm) may develop chronic pulmonary aspergillosis at sites of lung damage.
CXR: mobile, intracavitary mass w/ an air crescent in the periphery

45
Q

Invasive aspergillosis

A

Pts w/ severe immunocompromise (eg prolonged neutropenia, post transplant) are far more likely to develop invasive disease.
CT: nodules w/ surrounding ground-glass opacities (“halo sign”)

46
Q

Pneumonia + V/Q

A

Alveolar consolidation in pneumonia causes hypoxemia due to R to L intrapulmonary shunting.
Positonal changes that make the consolidation more gravity dependent worsent V/Q mismatch, increasing intrapulmonary shunting, and lead to worsened hypoxemia.

47
Q

Mechanical ventilation

Oxygenation influenced by FiO2 + Peep
PaCO2 influenced by respiratory rate and tidal volume

Prolonged high FiO2 can cause oxgen toxicity due to formation of O2 free radicals and predispose to atelectasis; levels less than <60% are safe; better to decrease FiO2 than PEEP for this reason

Decreasing PEEP would lower oxygenation by decreasing the number of alveoli avaiable for gas exchange, resulting in shunting.

A

Increased peak pressure assoc. w/ an unchanged plateau suggests a pathological process causing increased airway resistance, such as bronchospasm, mucus plug, or endotracheal tube obstruction.

Elevation of both peak and plateau pressures indicates a process causing decreased pulmonary compliance (pulmonary edema, atelectasis, pneumonia, or R mainstem intubation).

48
Q

What is alpha 1 antitrypsin deficiency?

A

Codominant genetic disease; family hx of emphysema or liver disease
Should be considered in pts w/ COPD at young age <45, COPD w/ minimal or no smoking hx, basilar predominant COPD, or hx of unexplained liver disease
Presents similarly to COPD
Chronic productive cough, dyspnea, wheezing, recurrent respiratory infection
Smokers present in their 30s; nonsmokers 40s
Smoking-induced centriacinar (centrilobar) emphysema: destruction of the upper lobes
Panacinar emphysema of AAT deficiency: destruction of lower lobes
Liver: neonatal hepatitis, hepatocellular carcinoma
-biopsy: periportal eosinophilic inclusion bodies
Skin: panniculitis
Dx: measurement of AAT levels, PFT
Tx: IV supplementation w/ human AAT in addition to bronchodilators and corticosteroids as needed
Severe lung disease: lung transplant, liver transplant

49
Q

Lung cancer and Hodgkin lymphoma.

A

Secondary malignancy is common in pts w/ HL treated w/ chemotherapy and radiation.
High risk of developing 2nd cancer in general, esp if treated before 30y.
The most common secondary solid tumor malignancies are lung (esp in smokers), breast, thyroid, bone, and GI (colorectal, esophageal, gastric tumors).

50
Q

Cystic fibrosis

A

Almost all men w/ CF have obstructive azoospermia from congenital absence of bilateral vas deferens.
The vas deferens fails to develop due to accumulation of inspissated mucus in the fetal genital tract, resulting in infertility.

51
Q

What is hypersensitivy pneumonititis?

A

Inflammation of the lung parenchyma caused by antigen exposure.
Acute episiodes present w/ cough, breathlessness, fever and malaise that occur w/in 4-6h of antigenic exposure.
Chronic exposure may cause wt loss, clubbing, and honeycombing of the lung.
XR: ground glass opacity or “haziness” of lower lung fields
Tx: avoidance of responsible antigen

52
Q

Exudative effusions

A

Inflammatory
Due to:
empyema, chylothorax, malignancy, TB, RA

53
Q

What is chylothorax?

A

Occurs when lymphatic flow through the thoracic duct is disrupted, leading to direct leakage to chyle (ie lymphatic fluid) into the pleural cavity
Contains triglycerides
Pleural fluid analysis: milky-white fluid w/ lymphocyte predominance and increased triglycerides
Mgmt: drainage via thoracentesis or chest tube placement, limitation of dietary fat, and possible thoracic duct ligation

54
Q

Transudative effusions

A
Result from oncotic or hydrostatic pressure differentials
Protein loss (eg nephrotic syndrome) results in decreased plasma oncotic pressures. 
Increased pulmonary vascular pressures (eg cardiac failure, pulmonary embolism) cause increased hydrostatic forces; both resulting in pleural effusions. 
Hepatic hydrothorax can also lead to transudative effusions when ascitic flluid flows from the diaphragm (higher pressure) into the pleural cavity (lower pressure).
55
Q

Ventilation perfusion scan

A

Alternate study to CT angio for patients w/ significant renal impairment, morbid obesity, and/or contrast allergy.

56
Q

What is bronchopulmonary dysplasia?

A

Chronic lung disease of the neonate
RF: prematurity, LBW, respiratory distress syndrome, mechanical ventilation
Causes persistent O2 requirement
Commonly seen in premature infants, especially those requiring prolonged mechanical ventilation or O2 supplementation.
Surfactant therapy does not prevent BPD development but may reduce mortality from it

57
Q

Bronchial rupture

A

Rapid, large air leak into chest tube drainage system and persistent pneumothorax/pneumomediastinum despite tube thoracostomy in setting of blunt chest trauma
Dx: bronchoscopy
Tx: operative repair

Quantity and rapidity of leaked air in esophageal rupture is significantly less than with bronchial rupture.

58
Q

Pulmonary embolism

surgery, cancer = RF
ppx dose of anticoagulation does not eliminate risk esp. in high risk populations

A

Classically presents w/ sudden-onset pleuritic chest pain, cough, and dyspnea.
Clear lungs on XR
Hemoptysis can occur as a result of pulmonary infarction.
CT: wedge shaped infarction (virtually pathognomonic)
RF: malignancy (prothrombotic state)
Tx: (for cancer pts) LMWH (eg enoxaparin, dalteparin) due to possible increased risk of malignancy related bleeding w/ direct Xa oral anticoags (rivaroxaban)

59
Q

Penetrating thoracic trauma + hemorrhage

A

Blood output >1500ml

Persistent hemorrhage: >200ml/h for >2h or continuous need for blood transfusion to maintain hemodynamic stability

60
Q

What is asbestosis?

A

Pneumoconiosis resulting from inhalation of particles involved in many industrial processes.
Progressive dyspnea, clubbing, and end-inspiratory crackles.
PFT: restrictive lung disease pattern w/ decreased lung volume, decreased diffusion lung capacity, and a normal FEV1/FVC
Pleural plaques on imaging are hallmark of disease

61
Q

What is a solitary pulmonary nodule?

A

> 0.8cm require additonal management or surveillance
Round opacity up to 3cm in diameter, surrounded by pulmonary parenchyma. >3 = mass
By convention, there must be no assoc. pleural effusion, adenopathy, or atelectasis.
Most incidentially discovered are benign.
When compared to previous XR, if stable in size for >=2 years malignancy is ruled out and no further testing is necessary.
Malignant nodules tend to double in size over the course of a month to a year.

62
Q

Lung sounds

A
Sound travels faster in solids or liquid than in air which results in increased intensity of breath sounds and increased tactile fremitus in pt w/ a consolidative process inside the lung (bacterial pneumonia)
If fluid (pleural effusion) or air (pneumothorax) is present just outside the lung in thoracic cavity, they act to insulate sounds and vibration originating from the lung leading to decreased breath sounds and decreased tactile fremitus. 
Dullness to percussion occurs in both pleural effusion and lung consolidation due to increase in tissue/fluid density compared to normal air-filled lung tissue. 
Hyperresonance to percussion is characteristic of an air filled thoracic cavity (pneuothorax or hyperinflated lung (emphysema))
63
Q

Lung damage in COPD

A

Characterized by progressive expiratory airflow limitation which causes air trapping:
Decreased vital capacity, lung distensibility, compliance
Increased functional residual and total lung capacity
FEV1 is disproportionately decreased as compared to vital capacity.
Alveolar capillary membrane (the site of respiratory gas exchange) is destroyed in COPD.

64
Q

What is acute bronchitis?

A

Most cases are viral, no fever or consolidation on XR
A common cause of cough that may be productive of purulent, blood tinged sputum.
Yellow/purulent sputum due to epithelial sloughing and not a sign of bacterial infection. Blood in sputum can occur due to inflammation and epithelial damage. Secretions are easily mobilized unlike in pneumonia.
URI infection is the typical etiology, and symptoms are usually self limiting.
Symptomatic treatment and close clinical follow-up are the best management strategies.

65
Q

Spontaneous pneumomediastinum

A

Severe coughing paroxsyms can increase intraalveolar pressure and cause air to leak into subcutaneous tissues (ie subcutaneous emphysema), resulting in spontaneous pneumomediastinum.
First step in mgmt: CXR to confirm diagnosis and r/o pneumothorax

66
Q

What is chronic bronchitis?

A

Chronic productive cough for >3= months in 2 consecutive years.
Smoking is leading cause.

67
Q

What is bronchiectasis?

A

Irreversible dilation and destruction of bronchi, resulting in chronic cough and inadequate mucus clearance.
Compared to chronic bronchitis, bronchiectasis is more likely assoc. w/ a hx of recurrent respiratory tract infections and chronic cough w/ daily production of copious mucopurulent sputum.

68
Q

Transfusion related acute lung injury (TRALI)

A

Refers to development of fever, hypotension, and noncardiogenic pulmonary edema w/in SIX hours of blood product administration.
B/c LV function is typically normal, pulmonary artery catheterization reveals normal or high cardiac index and normal or low PWCP.

69
Q

Theophylline toxicity

A

It can manifest as CNS stimulation (eg headache, insomnia, seizures), GI disturbances (eg n/v), and cardiac toxicity (arrhythmia)
Inhibition of the cytochrome oxidase system by other meds, diet, or underyling disease can alter its narrow therapeutic window.
Cipro is known to decrease clearance of theophylline.
Can measure serum levels to assess toxicity.

70
Q

Massive PE

A

PE: dyspnea, chest pain, tachycardia, hypoxia, clear lungs
Massive: Present w/ syncope and hemodynamic collapse - RV dysfunction: accentuated (loud pulmonic component of S2), elevated central venous pressure (eg high JVP), pleuritic chest pain, tachycardia
Acute massive PE thrombus results in abrupt increases in pulm vasc resistance and RV pressures, RV hypokinesis, dilation, and hypotension

71
Q

CHF exacerbation

A

Bibasilar crackles, respiratory alkalosis; fluid overload, S3 and S4 gallops, cardiomegaly

Exacerbation can cause tachypnea as LV dysfunction allows fluid to pool in the lungs, causing a pleural effusion and hypoxemia due to reduce ventilation.
Tachypnea causes hypocapnia and respiratory alkalosis.

72
Q

COPD exacerbation

A

Wheezing, respiratory acidosis due to CO2 retention
Characterized by change in >=1 of the following:
-cough severity or frequency
-volume or character of sputum production
-level of dypsnea
URI is the most common trigger of COPD exacerbation

73
Q

What is a superior pulmonary sulcus tumor/Pancoast tumor?

A

Usually malignant lung neoplasms (squamous cell carcinoma or adenocarcinoma)
Most commonly present w/ referred shoulder pain due to invasion of brachial plexus or adjacent structures
Other common findings: Horner syndrome (ptosis, miosis, anhydrosis), radicular pain, paresthesias, or weakness of the ipsilateral arm due to invasion of the brachial plexus

74
Q

Cystic fibrosis

A

Due to mutation in CFTR protein
Chronic rhinosinusitis due to thick, viscous secretions and impaired mucociliary clearance, leading to chronic sinopulmonary disease
Facial pain +/- Nasal polyps: bilateral, present as nontender, shiny, grey or yellow masses in nasal cavity or paranasal sinuses
Viscous secretions block pancreatic ducts leading to exocrine pancreas dysfunction
Decreased or absent pancreatic enzymes cause fat malabsorption w/ oily loose stools and FTT and/or wt loss
Over time, pancreatic insufficiency can lead to impaired glucose intolerance and CF related DM

75
Q

Primary ciliary dyskinesia

A

Can present similarly to CF w/ chronic rhinosinusitis and nasal polyposis due to impaired mucociliary clearance.

However, GI system is NOT affected.

76
Q

Low glucose in exudative pleural effusion

A

Glucose concentration in empyema is decreased due to high metabolic acivity of leukocytes (and/or bacteria) in the fluid.

77
Q

Positve pressure ventilation

A

PPV is sometimes used to help open collapsed alveoli and improve atelectasis.
But it does not help address PEs.

78
Q

Noninvasive positive pressure ventilation (NPPV)

A

Use in pt w/ acute exacerbation of COPD has been shown to decrease mortality, rate of intubation, hospital length of stay, and incidence of nosocomial infection.
Endotrachael intubation w/ mechanical ventilation is recommended for pts who fail a trial of NPPV.

79
Q

Acute nitrofurantoin-induced pulmonary injury

A

Due to a hypersensitivity pneumonitis that can present w/ fevers, shortness of breath, dry cough, erythematous rash.
Erythematous, maculopapular rash may be present
Pleural effusions also occur and are typically unilateral
Symptoms usually begin 3-9d from med initiation.
Bilateral basilar opacities and pleural effusions are common.
Long-term use can lead to interstitial lung disease
Labs: leukocytosis, eosinophilia
Tx: cessation of nitrofurantoin (macrobid)

80
Q

Mechanical ventilaton + ARDS

A

Use of low tidal volume ventilation (6ml/kg of ideal body weight) decreases likelihood of overdistending alveoli and provoking barotrauma due to high plateau pressures (pressure applied to small airways and alveoli)
O2:
-Increasing FiO2 administed by ventilator improves oxygenation, however prolonged FiO2 levels >0.6 are assoc. w/ O2 toxicity
-Increasing PEEP (15-20cm H20) also improves oxygenation by preventing alveolar collapse at the end of expiration, thereby decreasing shunting and the work of breathing
Goal: PaO2 55-80 preventing SpO2 <88

81
Q

Drowning

A

Defined as respiratory impairment after submersion in liquid.
Aspirated liquid causes hypoxemia and can wash out pulmonary surfactant, leading to insidious onset of acute respiratory distress syndrome (aka respiratory insufficiency).

Pneumonia can complicate drowing when the pt is submerged in contaminated water (eg lake) but is less likely following submersion in a swimming pool.

82
Q

Pulmonary HTN

A

Elevated pulmonary artery and right atrial pressures

83
Q

Pulmonary capillary wedge pressure

A

Reflects left atrial pressure and left sided heart function.
An elevated PCWP combined w/ elevated R-sided pressures suggests L-sided HF leading to R-sided HF.

However, normal PCWP reflects normal LV function, suggesting elevated pulmonary pressures are due to an intrinsic pulmonary process.

84
Q

Postop risk

A

COPD, OSA, active smoking, obesity, and advanced age are risk factors for postoperatie pulmonary complications such as pneumonia.
Preoperative physical therapy helps reduce the postop risk of pneumonia and shortens postop hospital stay.

85
Q

Tracheobronchial injury

A

Should be considered in pts w/ thoracic trauma and extensive extrapulmonary air (eg chest tube w/ persistent large air leak)
Bronchoscopy can confirm the dx prior to operative repair
It can be easily performed through the endotracheal tube in intubated patients
High res CT scan can diagnose major injuries but may miss small tears