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Assessment '24 - Mordecai > T4 - Restrictive Lung Disease > Flashcards

T4 - Restrictive Lung Disease Flashcards

1
Q

Restrictive lung disease affects these two things…

A

Lung expansion and compliance
RLD is typically r/t connective tissue diseases, environmental factors, pulmonary fibrosis, conditions that increase alveolar or interstitial fluid, and diseases that limit excursion of the chest/diaphragm

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2
Q

What is the hallmark of RLD?

A

Inability to increase lung volume in proportion to an increase in alveolar pressure
…these disorders lead to reduced surface area for gas diffusion, causing V/Q mismatching and hypoxia

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3
Q

As lung elasticity worsens, pts become symptomatic d/t (3)

A

Hypoxia, inability to clear secretions, and hypoxia

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4
Q

Effects of RLD on FEV, FEV1, and FEV1:FVC ratio

A

↓FEV
↓FVC
↔/↑FEV1:FVC ratio
…also, a reduced diffusion capacity for carbon monoxide (DLCO)

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5
Q

Effects of RLD on lung volumes

A

All lung volumes are decreased, especially total lung capacity (TLC)

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6
Q

Expected changes in the volume flow loop

A
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7
Q

What is the principal feature of RLD, represented in spirometry

A

TLC

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8
Q

TLC is used to classify RLD as mild, moderate, or severe. What are the % of predicted value ranges?

A

Mild: TLC 65-80%
Moderate: TLC 50-65%
Severe: TLC <50%

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9
Q

List of RLD causes

A
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10
Q

What is the cause of pulmonary edema? Acute pulmonary edema?

A

Interstitial fluid leakage into the interstitium & alveolar space
Acute pulmonary edema can be c/b increased capillary pressure or by increased capillary permeability
…both lead to “capillary stress failure”

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11
Q

What characteristics does a CXR showing pulmonary edema have?

A

Bilateral, symmetric perihilar opacities
…butterfly fluid pattern, more commonly seen w/increased capillary pressure than increased capillary permeability

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12
Q

Diffuse alveolar damage, typically present with increased-permeability pulmonary edema, is associated with _______

A

ARDS

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13
Q

Pulmonary edema c/b increased capillary permeability is characterized by ↑ or ↓ concentration of protein and secretory products in the edema fluid.

A

↑

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14
Q

With what kinds of heart failure (2) can cardiogenic pulmonary edema be present?

A

Acute & decompensated

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15
Q

What are the characteristics of cardiogenic pulmonary edema? (4)

A

Dyspnea
Tachypnea
Elevated cardiac pressures
SNS activation

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16
Q

What conditions increase the risk of cardiogenic pulmonary edema? (vague answer)

A

Conditions that acutely increase preload s/a acute aortic regurgitation and acute mitral regurgitation
Conditions that increase afterload or SVR s/a LV outflow tract obstruction, mitral stenosis, and reno-vascular HTN

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17
Q

Negative pressure pulmonary edema (post-obstructive pulmonary edema) results after the relief of an acute upper airway obstruction; what are the causes? (6)

A

Laryngospasm
Epiglottitis
Tumors
Obesity
Hiccups
OSA
…onset after relief of obstruction ranges from a few minutes to 2-3hrs

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18
Q

Treatment for negative pressure pulmonary edema

A

Supplemental O2 and maintenance of a patent upper airway, this form of pulmonary edema is typically self-limited
Mechanical ventilation may occasionally be needed for a brief period

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19
Q

Common signs of negative pressure pulmonary edema

A

Tachypnea
Cough
Failure to maintain SpO2 >95%
….can be confused with aspiration or pulmonary embolism

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20
Q

Pathogenesis of negative pressure pulmonary edema

A

Spontaneous ventilation is necessary to create negative pressure, drawing in fluid. High negative intrapleural pressure is developed against an obstructed upper airway, and negative intrapleural pressure decreases interstitial hydrostatic pressure, increases venous return, and increases left ventricular afterload. These factors produce acute pulmonary edema by increasing the transcapillary pressure gradient.

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21
Q

Pathogenesis of neurogenic pulmonary edema

A

Develops in a small fraction of acute brain injury patients, Occurs minutes-hours after CNS injury and may manifest during the period period. Massive outpouring of SNS impulses from the injured CNS that results in generalized vasoconstriction and blood volume shift into the pulmonary circulation. The increased pulmonary capillary pressure c/b translocation of the blood volume leads to the transfer of fluid into the interstitium and alveoli.

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22
Q

Pathogenesis of re-expansion pulmonary edema (REPE)

A

The rapid expansion of a collapsed lung may lead to REPE

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23
Q

The risk of REPE after relief of a pneumothorax or pleural effusion is related to:

A
  1. amount of air/liquid that was in the pleural space (>1 increases risk)
  2. the duration of collapse (>24 hrs increases the risk)
  3. speed of re-expansion
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24
Q

Treatment for REPE

A

Supportive care

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25
Q

What two drugs are especially risky for causing drug-induced pulmonary edema?

A

Opioids (heroin)
Cocaine - causes pulmonary vasoconstriction, acute myocardial ischemia, and myocardial infarction

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26
Q

A _____ protein concentration of pulmonary edema fluid suggests a ______ permeability pulmonary edema

A

high
high

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27
Q

Can naloxone be used to treat opioid-induced pulmonary edema?

A

There is no evidence to support this

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28
Q

If pulmonary edema on chest x-ray does not respond to diuretics, what other condition might be present?

A

Diffuse alveolar hemorrhage (DAH)

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29
Q

Treatment of drug-induced pulmonary edema

A

Supportive
Intubation and mechanical ventilation

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30
Q

Heights causing high-altitude pulmonary edema (HAPE) and influencing factors

A

2500-5000m
Influenced by the rate of ascent to that altitude

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31
Q

Onset of high-altitude pulmonary edema (HAPE)

A

Onset is often gradual but typically occurs within 48-72 hours at high altitude
Sudden pulmonary edema may be preceded by less severe symptoms of acute mountain sickness

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32
Q

Treatment of high-altitude pulmonary edema (HAPE)

A

O2 administration and quick descent to lower altitude
Inhalation of nitric oxide may improve oxygenation

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33
Q

Anesthetic implications w/pulmonary edema

A

Elective surgery should be delayed
Optimize cardiorespiratory function before surgery

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34
Q

Anesthetic implications w/pleural effusion

A

Large pleural effusions may need to be drained

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35
Q

Anesthetic implications w/hypoxemia

A
  • Mechanical ventilation and PEEP
  • Current evidence shows benefit from ventilation using low TV & RR of 14-18 while attempting to keep end-inspiratory plateau pressure <30 cmH2O
  • Careful titration of PEEP in conjunction with inspiratory pause is recommended to optimize lung compliance
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36
Q

Breathing patterns with restrictive lung disease

A
  • Rapid, shallow breathing
  • Tachypnea should not be used as the sole criteria for delaying extubation if gas exchange and other assessments are satisfactory
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37
Q

Chemical pneumonitis sx:

A

Abrupt onset dyspnea, tachycardia, and decreased SP02

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38
Q

Pathogenesis of aspiration pneumonitis

A
  • Pts w/ decreased airway reflexes are at risk for aspiration
  • When gastric fluid is aspirated, it distributes throughout the lungs and destroys surfactant-producing cells and pulmonary capillary endothelium
  • As a result, there is atelectasis and leakage of intravascular fluid into the lungs, producing capillary-permeability pulmonary edema
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39
Q

Evidence of aspiration pneumonitis

A
  • CXR may not demonstrate evidence of aspiration pneumonitis for 6-12 hrs
  • Evidence of aspiration is most likely in the superior segment of the RLL if the pt aspirated in the supine position
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40
Q

Interventions for chemical pneumonitis

A
  • Many CRNA’s recommend keeping the HOB elevated for intubation & extubation to decrease aspiration risk
  • If aspiration noted, the oropharynx should be suctioned and the pt turned to the side
  • T-burg position will not stop gastric reflux, but can prevent aspiration once gastric contents are in the pharynx
  • After an episode, pts may need to be monitored for 24-48 hrs
    Measurement of gastric fluid pH is useful, since it reflects the pH of the aspirated fluid
  • The aspirated gastric fluid is also rapidly redistributed to peripheral lung regions, so lavage is not useful unless there has been an aspiration of particulate material
  • Aspiration pneumonitis is best treated w/ supplemental 02 & PEEP
  • Bronchodilation may be needed to relieve bronchospasm
  • There is no evidence that abx decreases the incidence of pulmonary infection or alter outcomes
  • Abx may be considered if a pt symptomatic after 48 hrs and + culture results
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41
Q

Tx for E-Cigarette (vaping) –associated lung injury (EVALI)

A

Antibiotics, systemic steroids, and supportive care are the mainstays of therapy

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42
Q

Sx for E-Cigarette (vaping) –associated lung injury (EVALI)

A

Dyspnea, cough, N/V/D, abd pain, and pleuritic or nonpleuritic chest pain
Pt may be febrile, tachycardia, tachypnea, and hypoxic

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43
Q

What is the most commonly reported finding and it directly r/t the severity of initial disease process in COVID-19

A

A drop in diffusion capacity

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44
Q

Who is at the highest risk for long-term pulmonary complications r/t COVID-19?

A

Pts who need mechanical ventilation

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45
Q

What is acute respiratory failure?

A

When the Pa02 is <60 mmHg despite 02 supplementation and in the absence of a right-to-left intracardiac shunt

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46
Q

What change occurs with PaCO2 in ARF?

A
  • PaC02 can be increased, unchanged, or decreased d/o the relationship of alveolar ventilation to C02
  • A production PaC0 >50 mmHg in the absence of respiratory-compensated metabolic alkalosis is consistent with the diagnosis of ARF
  • ARF is distinguished from chronic respiratory failure based on the relationship of PaC02 to arterial pH, ARF is typically accompanied by abrupt increases in PaC02 and decreases in pH
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47
Q

3 tx goals of ARF:

A

1) a patent airway 2) hypoxemia correction 3) removal of excess C02

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48
Q

What PaO2 level corresponds with an adequate PsO2 of >90%?

A

> 60 mmHg

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49
Q

What is volume-cycled ventilation (VCV):

A

Fixed TV w/inflation pressure as dependent variable

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50
Q

What are the primary modes of VCV? (2)

A

Assisted/controlled ventilation (A/C) and synchronized intermittent mandatory ventilation (SIMV)

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51
Q

What vent mode has a set RR ensuring the number of breaths even if there is no inspiratory effort? If negative pressure is sensed, a tidal volume will be delivered.

A

A/C ventilation

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52
Q

What vent mode allows SV, while providing a predefined minute ventilation? The circuit provides sufficient gas flow and periodic mandatory breaths that are synchronous with the pt’s inspiratory efforts

A

SIMV

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53
Q

Advantages of SIMV over A/C include

A

continued use of respiratory muscles, lower mean airway and mean intrathoracic pressure, prevention of respiratory alkalosis, and improved pt–ventilator coordination

54
Q

What vent mode provides gas flow to the lungs until a preset airway pressure is reached? Tidal volume is the dependent variable and varies with changes in compliance and airway resistance

A

Pressure-cycled ventilation

55
Q

In mechanically ventilated pts w/acute respiratory failure, ____________ is the most important predisposing factor for developing nosocomial pneumonia (ventilator-associated pneumonia)
The primary cause is _____________ of contaminated secretions around the ETT cuff

A

Intubation
Micro-aspiration

56
Q

Tx of nosocomial sinusitis includes:

A

Antibiotics, replacement of nasal tubes with oral tubes, decongestants and head elevation to facilitate sinus drainage

57
Q

Barotrauma presenations:

A

May present as subcutaneous emphysema, pneumomediastinum, pulmonary interstitial emphysema, pneumoperitoneum, pneumopericardium, arterial gas embolism, or tension pneumothorax
…Infection increases the risk of barotrauma, by weakening pulmonary tissue

58
Q

What is a common cause of hypoxemia during mechanical ventilation?

A

Ateletasis

59
Q

T/F: Hypoxemia d/t atelectasis is responsive to an increase in Fi02

A

False
Bronchoscopy may be necessary to remove mucous plugs

60
Q

Complications of mechanical ventilation, changes in PaO2, PaCO2, and response to supplemental oxygen

A
61
Q

Significant desaturation of arterial blood occurs only when the Pa02 is

A

< 60mmHg

62
Q

3 main causes of arterial hypoxemia

A

V/Q mismatch, *right-to-left pulmonary shunting, and hypoventilation
Only condition not likely to improve with increased O2

63
Q

Compensatory responses are also present in chronic hypoxemia when Pa02 is <50 These responses include:

A
  1. Carotid body–induced increase in alveolar ventilation
  2. Hypoxic pulmonary vasoconstriction to divert pulmonary blood flow away from hypoxic alveoli
  3. Increased SNS activity to increase COP and enhance tissue oxygen delivery
64
Q

Chronic hypoxemia leads to an _________ in RBC mass to improve 02-carrying capacity

A

Increase

65
Q

Normally the VD:VT is _____, but it may increase to _____ when there is an increase in dead space ventilation

A

< 0.3
≥ 6
An increased VD:VT occurs in the presence of ARF, a decreased COP, and pulmonary embolism

66
Q

Hypercarbia is defined as a PaC02….

A

> 45 mmHg

67
Q

Acute increases in PaC02 are assoc w/ _______ CBF and ICP

A

Increased

68
Q

What is permissive hypercapnia?

A

A strategy of allowing PaC02 to increase to ≥55 to avoid or delay the need for intubation & ventilation

69
Q

Extreme increases in PaC02 to ________ result in CNS depression

A

> 80mmHg

70
Q

The difference btw mixed venous partial pressure of oxygen (Pv02) and arterial venous oxygen (Ca02 − Cv02) reflects….

A

Overall adequacy of COP relative to tissue oxygen extraction

71
Q

Acidosis is often associated with arterial ____________
Alkalemia is often associated with mechanical __________ and diuretic use

A

Hypoxemia
Hyperventilation

72
Q

Dysrhythmias may be increased by respiratory _______

A

alkalosis

73
Q

Right-to-left pulmonary shunting:

A

Perfusion of nonventilated alveoli

74
Q

Net effect of right-to-left pulmonary shunting

A

A decrease in Pa02, reflecting the dilution of oxygenated blood with hypo-oxygenated blood coming from unventilated alveoli

75
Q

A physiologic shunt typically accounts for _______ of COP

A

2-5%

76
Q

Guidelines that have been proposed for discontinuing mechanical ventilation include:

A
  • Vital capacity of >15 mL/kg
  • Alveolar-arterial oxygen difference of <350 cmH2O while breathing 100% 02
  • Pa02 of >60 mmHg with an Fi02 of <50%
  • Negative inspiratory pressure of more than −20 cmH2O
  • Normal pHa
  • RR <20
  • VD:VT of < 0.6
77
Q

When a pt is ready for a trial of vent withdrawal, 3 options may be considered:

A
  1. SIMV, which allows progressively fewer mandatory breaths until pt breathing on their own
  2. Intermittent trials of total removal of mechanical support and breathing through a T-piece
  3. Use of decreasing levels of pressure support ventilation
78
Q

Several things may interfere with successful extubation:

A
  • Excessive workload on the respiratory muscles d/t hyperinflation, copious secretions, bronchospasm, increased lung water, or increased C02 production
  • Noninvasive ventilation (NIV) may be considered as a bridge
79
Q

Extubation should be considered when pts tolerate _____min of SV with CPAP of ___ cm H2O without deterioration in ABGs, mental status, or cardiac function

A

30
5

80
Q

For Extubation:
The Pa02 should remain ________ with Fi02 <50%
PaC02 should remain ________ and the pHa >7.30

A

> 60mmHg
< 50 mmHg

81
Q

For extubation:
Additional criteria include PEEP _____cmH2O, RR _____, and VC _____ mL/kg

A

< 5
< 20
> 15

82
Q

What is the highest risk of ARDS?

A

Sepsis

83
Q

Hallmark of ARDS:

A

Rapid-onset respiratory failure, arterial hypoxemia, and CXR findings similar to cardiogenic pulmonary edema

84
Q

Tx for ARDS:

A

Supportive care consists of ventilation, antibiotics, stress ulcer prophylaxis, DVT prophylaxis, and early enteral feeding

85
Q

ARDS management:

A
  • Prone positioning and extracorporeal membrane oxygenation (ECMO) have been proposed as therapies for the life-threatening refractory hypoxemia
  • Prone positioning exploits gravity and repositioning of the heart in the thorax to recruit lung units and improve V/Q matching
  • ECMO can be considered in pts with severe hypoxemic and/or hypercapnic respiratory failure as a possible rescue therapy
  • The aim of this strategy is to rest the lungs until severe hypoxemia, and respiratory acidosis has resolved
  • Additional supportive therapies: Optimal fluid mgmt, NMB, inhaled nitric oxide, prostacyclins (PGI2), recruitment maneuvers, surfactant replacement, glucocorticoids, and ketoconazole
86
Q

ILD (interstitial lung disease) examples:

A

Sarcoidosis
Hypersensitivity Pneumonia
Pulmonary Langerhans Cell Histiocytosis
Pulmonary Alveolar Proteinosis
Lymphangioleiomyomatosis

87
Q

Presentation of ILD

A

Pts usually present with dyspnea & nonproductive cough
Pulmonary htn & cor pulmonale develop as progressive pulmonary fibrosis causes loss of pulmonary vasculature

88
Q

ILD presentation in the hands

A

Digit clubbing

89
Q

Sarcoidosis

A

Systemic granulomatous disorder that involves many tissues, most commonly in the lungs and intrathoracic lymph nodes

90
Q

What is the most common form of neurologic sarcoidosis?

A

Unilateral facial nerve palsy

91
Q

Which enzyme activity is increased w/sarcoidosis, likely d/t its production by granuloma cells?

A

Angiotensin-converting enzyme

92
Q

What test is used to detect sarcoidosis and is similar to a tuberculin test?

A

Kveim test

93
Q

Tx to suppress sx of sarcoidosis and treat hypercalcemia

A

Corticosteroids

94
Q

Hypersensitivity pneumonitis

A

Characterized by diffuse interstitial granulomatous in the lungs after inhalation of dust containing fungi, spores, animal or plant material

95
Q

Sx of hypersensitivity pneumonitis

A

Dyspnea & cough 4-6 hrs after inhailing the antigen, followed by leukocytosis, eosinophilia, and often arterial hypoxemia

96
Q

CT findings of hypersensitivity pneumonitis

A

CT shows ground-glass opacities in the mid to upper lung zones

97
Q

Tx for hypersensitivity pneumonitis

A

Treatment consists of antigen avoidance, glucocorticoids, and lung transplant

98
Q

Pulmonary LangerhansCell Histiocytosis

A

In this disease the inflammation is usually around smaller bronchioles, causing destruction of the bronchiolar wall and surrounding lung parenchyma

99
Q

Pulmonary Langerhanscell histiocytosis is associated with what bad habit?

A

Smoking tobacco

100
Q

Findings associated with pulmonary Langerhanscell histiocytosis

A
  • The disease usually affects the upper and middle zones of the lung
  • CT can be diagnostic, showing cysts or honeycombing in upper zones with costophrenic sparing
  • Lung biopsy shows inflammatory lesions around the bronchioles containing Langerhans cells, eosinophils, lymphocytes, and neutrophils
101
Q

Tx for pulmonary Langerhanscell histiocytosis

A

Smoking cessation, systemic glucocorticoids, and symptomatic support

102
Q

Pulmonary Alveolar Proteinosis (PAP)

A
  • Disease characterized by lipid-rich proteinaceous materials in the alveoli
  • It usually presents in the fourth or fifth decade of life w/ sx of dyspnea and hypoxemia
103
Q

What condition is associated with CXR batwing distribution of alveolar opacities in middle and lower lung zones?

A

Pulmonary Alveolar Proteinosis (PAP)

104
Q

Lymphangioleiomyomatosis

A

Rare multisystem disease that results in proliferation of smooth muscle in airways, lymphatics, and blood vessels mostly in women of reproductive age

105
Q

Tx for Lymphangioleiomyomatosis

A

Sirolimus (immunosuppressive) is indicated in symptomatic pts w/progressive disease

106
Q

Aging effects on the lungs

A

Physiologic lung changes, decreased chest wall compliance, and decreased elastic recoil

107
Q

Changes to RV, VC, FRC, FEV1/FV and FVC

A

↑ RV
↓ VC
↑ FRC
↓ FEV1/FVC

108
Q

Chronic Extrinsic Restrictive Lung Disease

A

Chronic extrinsic restrictive lung disease is often d/t disorders of the thoracic cage (chest wall) that interfere with lung expansion

109
Q

Causes of thoracic extrapulmonary chronic extrinsic restrictive lung disease

A

Deformities of the sternum, ribs, vertebrae, & costovertebral structures include: ankylosing spondylitis, flail chest, scoliosis, and kyphosis

110
Q

2 types of costovertebral skeletal deformities causing chronic extrinsic restrictive lung disease

A

Scoliosis & kyphosis

111
Q

Pectus carinatum

A

Aka “pigeon chest:” deformity of sternum characterized by the outward projection of the sternum & ribs
- Usually more of a cosmetic concern, but may cause respiratory symptoms or asthma

112
Q

What can cause a flail chest w/paradoxic inward movement of the unstable portion of the thoracic rib cage?

A

Multiple rib fractures

113
Q

Pleural effusion

A

Fluid (blood, serous fluid, pus, lipids) in pleural space
Dx made with CXR, CT, or bedside US (preferred)

114
Q

Pneumothorax

A

Gas in the pleural space c/b disruption the parietal pleura or visceral pleura. May be spontaneous or secondary to pathology

115
Q

Idiopathic spontaneous PTX

A

Occurs most often in tall, thin men age 20-40 and is c/b rupture of apical subpleural blebs

116
Q

Secondary PTX

A

May occur as a complication ofCOPD, pulmonary malignancies, cystic fibrosis, or lung abscesses

117
Q

Tensionptx

A

Medical emergency and develops when gas enters the pleural spaceduring inspiration andcan’tescaping during exhalation

118
Q

Pleural fibrosis

A

May follow hemothorax, empyema, or surgical pleurodesis
Functional restrictive lung abnormalities are usually minor. Surgical decortication to remove thick fibrous pleura is considered if the restrictive lung disease is very symptomatic.

119
Q

Acute mediastinitis

A

c/b bacterial contamination after esophageal perforation
Symptoms include chest pain & fever. It is treated with broad-spectrum abx & surgical drainage

120
Q

Mediastinal masses

A
  • Anterior mediastinal masses: thymomas (20%, most common), germ cell tumors, lymphomas, intrathoracic thyroid tissue, & parathyroid lesions
  • Middle mediastinal masses: tracheal masses, bronchogenic and pericardial cysts, enlarged lymph nodes, and proximal aortic disease (i.e., aneurysm or dissection)
  • Posterior mediastinal masses: neurogenic tumors and cysts, meningoceles, lymphomas, descending aortic aneurysms, and esophageal disorders such as diverticula and neoplasms
121
Q

Tx of mediastinal mass

A
  • Many require surgery, radiation, chemotherapy, or careful surveillance over time
  • Preop evaluation includes measurement of a flow-volume loop, chest imaging, and clinical evaluation for evidence of airway compression
122
Q

Asphyxiating thoracic dystrophy

A

“Jeune syndrome:” autosomal recessive disorder with skeletal dysplasia and multiorgan dysfunction

123
Q

Fibrodysplasia ossificans

A

Hereditary disorder c/b a genetic variation in bone morphogenetic protein (BMP) type 1

124
Q

Poland syndrome

A

Partial or complete absence of pectoral muscles, commonly affecting one side. Pts may also have paradoxic respiratory motion due to the absence of multiple ribs.

125
Q

3 neuromuscular disorders associated with respiratory compromise

A

Guillian-Barre syndrome
Myasthenia gravis
Muscular dystrophy

126
Q

In quadriplegic pts w/ injury below T4, breathing is maintained solely or predominantly by the __________

A

Diaphrgam

127
Q

Changes in FEV1, FVC, FRC, and ERC
….changes to RV and TLC w/BMI >40

A

↓FEV1
↓FVC
↓FRC
↓ERV
↓RV
↓TLC

128
Q

Ways in which pregnancy can lead to restrictive lung physiology

A
  • Subcostal angle of the rib cage and the circumference of the lower chest wall increase and the diaphragm moves cephalad
  • Increased levels of relaxin cause stretching of the lower rib cage ligaments
  • The subcostal angle widens
  • The anteroposterior diameter and transverse diameter of the chest wall increases, leading to an increase in the rib cage circumference
  • These changes peak at the 37th week of pregnancy
  • Chest wall configuration normalizes about 6 months postpartum, except for the subcostal angle, which remains wider by about 20%
  • The enlarging uterus pushes the diaphragm up by about 4 cm
129
Q

Which form of bronchoscopy is more generally used? Fiberoptic or rigid?

A

Fiberoptic

130
Q

What is a major contraindication to pleural biopsy?

A

Coagulopathy

Assessment '24 - Mordecai (10 decks)

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