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ACVECC Top 100(?) Papers > Respiratory > Flashcards

Respiratory Flashcards

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1
Q

According to Hung et al. (2016), what was the typical volume and nature of pleural fluid in healthy dogs with thoracostomy tubes?

A

In healthy dogs with thoracostomy tubes, Hung et al. (2016) found that a small amount of serosanguinous pleural fluid accumulated (median ~4.3 mL/kg/day), characterized cytologically as a transudate with minimal inflammation.

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2
Q

According to Pang et al. (2007), how accurate is intranasal EtCO₂ as a surrogate for PaCO₂ in dogs?

A

Pang et al. (2007) reported that intranasal EtCO₂ correlates moderately with PaCO₂ in dogs (mean difference ~5 mmHg), but is not reliable enough to replace arterial sampling due to variability and underestimation of hypercapnia.

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3
Q

In the 2019 PETAL trial, what effect did early neuromuscular blockade (NMB) have on mortality in ARDS patients?

A

The PETAL trial found that early NMB with cisatracurium did not significantly reduce 90-day mortality compared to usual care, though it was associated with fewer ventilator days in some subgroups.

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4
Q

What CT findings were most commonly associated with surgical findings in dogs with pyothorax, per Swinbourne et al. (2011)?

A

CT most commonly revealed pleural effusion, gas pockets, and enhancing pleural thickening. However, accuracy for identifying the exact lesion requiring thoracotomy was limited.

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5
Q

According to Thompson et al. (2017), what are the core diagnostic criteria for ARDS in humans?

A

ARDS is diagnosed by acute onset (<1 week), bilateral pulmonary infiltrates not explained by cardiac failure, PaO₂/FiO₂ ≤300 mmHg on PEEP ≥5 cm H₂O, and origin of edema from increased permeability.

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6
Q

What are the pathophysiologic hallmarks of ARDS according to Thompson et al. (2017)?

A

Hallmarks include diffuse alveolar damage, loss of surfactant, inflammatory cell infiltration, and alveolar-capillary barrier disruption, leading to severe hypoxemia and decreased lung compliance.

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7
Q

According to Aggarwal et al. (2018), what outcome was associated with oxygen tensions exceeding protocol goals in ARDS?

A

Higher arterial oxygen tensions (PaO₂ >80 mmHg) were associated with worse outcomes, including increased mortality, suggesting harm from hyperoxia in ARDS.

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8
Q

What was the main finding of De Monte et al. (2018) regarding tidal volume in anesthetized healthy dogs?

A

Low tidal volume (6 mL/kg) ventilation with PEEP reduced lung strain and prevented atelectasis compared to high tidal volume (15 mL/kg), supporting lung-protective strategies even in healthy lungs.

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9
Q

According to Lappin et al. (2017), what antimicrobials are recommended for uncomplicated canine bronchitis?

A

Doxycycline (5–10 mg/kg q12–24h) is first-line due to activity against Bordetella and Mycoplasma. Culture is recommended in non-responders or complex cases.

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10
Q

According to Bos & Ware (2022), what are the proposed phenotypes of ARDS?

A

Phenotypes include hyperinflammatory (high cytokines, shock, worse outcomes) and hypoinflammatory (less systemic involvement), which may respond differently to therapies.

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11
Q

Define the pathophysiologic difference between hypoinflammatory and hyperinflammatory ARDS phenotypes per Bos & Ware (2022).

A

Hyperinflammatory ARDS is marked by elevated IL-6, IL-8, and TNF-α, higher vasopressor and ventilation needs, and poorer prognosis; hypoinflammatory ARDS has lower inflammation markers and better outcomes.

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12
Q

What did the 2020 NEJM trial on conservative oxygen therapy in ICU patients conclude?

A

Conservative oxygen therapy (SpO₂ goal 90–97%) did not significantly reduce mortality compared to liberal oxygen, but reduced episodes of severe hyperoxia.

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13
Q

What were the findings of the NEJM (2020) study comparing liberal vs conservative oxygen in ARDS?

A

The trial showed no significant difference in 28-day mortality between liberal and conservative oxygen targets, though conservative therapy trended toward fewer adverse events.

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14
Q

According to Gorman et al. (2022), what are common long-term sequelae of ARDS?

A

Cognitive impairment, reduced pulmonary function (esp. DLCO), PTSD, neuromuscular weakness, and decreased quality of life are common long-term consequences of ARDS.

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15
Q

According to Luis Fuentes et al. (2019), how are feline cardiomyopathies classified?

A

Cardiomyopathies in cats are classified as hypertrophic, restrictive, dilated, arrhythmogenic, unclassified, and non-specific phenotypes based on echocardiographic and histopathologic features.

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16
Q

What are the pathophysiologic drivers of feline HCM per Luis Fuentes et al. (2019)?

A

Feline HCM is characterized by myocyte hypertrophy, disarray, fibrosis, and diastolic dysfunction. Secondary neurohormonal activation and elevated filling pressures contribute to clinical signs.

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17
Q

According to Reinero et al. (2019), what is the recommended diagnostic approach for pulmonary hypertension (PH) in dogs?

A

Diagnosis involves echocardiography (TR velocity >3.4 m/s), ruling out left heart disease, and assessing for underlying causes such as pulmonary disease, thromboembolism, or congenital shunts.

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18
Q

What is the mechanism of pulmonary hypertension in left-sided heart failure per Reinero et al. (2019)?

A

Chronic LA pressure elevation causes post-capillary PH via pulmonary venous congestion, endothelial dysfunction, and vascular remodeling, increasing RV afterload.

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19
Q

What are the key pathophysiologic processes of anaphylaxis per Smith et al. (2020)?

A

Anaphylaxis involves IgE-mediated mast cell degranulation, leading to vasodilation, increased vascular permeability, bronchoconstriction, and systemic hypotension.

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20
Q

What prognostic factors were associated with mortality in canine anaphylaxis per Smith et al. (2020)?

A

Factors included prolonged hypotension, bradycardia, delayed treatment, and requirement for vasopressors. Prompt epinephrine administration improved outcomes.

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21
Q

Define: Positive End-Expiratory Pressure (PEEP).

A

PEEP is the pressure in the lungs (above atmospheric) that remains at the end of expiration during mechanical ventilation, preventing alveolar collapse and improving oxygenation.

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22
Q

Define: Driving Pressure in mechanical ventilation.

A

Driving pressure = Plateau Pressure – PEEP. It reflects lung compliance and is a key determinant of ventilator-induced lung injury risk.

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23
Q

Define: Ventilator-Induced Lung Injury (VILI).

A

VILI refers to alveolar damage caused by overdistension (volutrauma), cyclic opening/closing (atelectrauma), and inflammation (biotrauma) during mechanical ventilation.

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24
Q

Define: Dead space ventilation.

A

Ventilation that does not participate in gas exchange due to alveolar or anatomic mismatch (e.g., embolism, overdistension). Measured via PaCO₂–EtCO₂ gradient.

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25
What is the physiologic rationale for lung-protective ventilation in ARDS?
Low tidal volumes (6 mL/kg) reduce volutrauma, maintain alveolar recruitment with PEEP, and minimize inflammatory mediator release, improving survival in ARDS.
26
What is the rationale for using high PEEP strategies in ARDS management?
High PEEP helps maintain alveolar recruitment, reduces atelectrauma, improves oxygenation, and minimizes ventilator-induced lung injury by stabilizing alveoli during expiration.
27
What is the downside of high PEEP strategies in ARDS patients?
Excessive PEEP can cause overdistension of alveoli (volutrauma), reduced venous return (decreased preload), hypotension, and increased dead space ventilation.
28
What did the ALVEOLI trial (ARDSNet) find when comparing high vs low PEEP strategies?
The ALVEOLI trial found no significant difference in mortality between high and low PEEP groups, but high PEEP improved oxygenation and reduced driving pressures in some patients.
29
How is driving pressure used to guide ventilation in ARDS?
Driving pressure (ΔP = Pplat – PEEP) is a surrogate for lung strain; values <15 cm H₂O are associated with better survival. It reflects compliance and lung protection more accurately than tidal volume alone.
30
What are the 'open lung' and 'lung rest' strategies in ARDS?
Open lung' aims to recruit and maintain alveoli with recruitment maneuvers + PEEP; 'lung rest' minimizes further injury by accepting permissive atelectasis, using lower tidal volumes and minimal PEEP.
31
Define oxygen toxicity and its key pathophysiologic mechanism.
Oxygen toxicity is tissue injury due to prolonged exposure to high FiO₂ (>60%), leading to formation of reactive oxygen species (ROS), lipid peroxidation, mitochondrial dysfunction, and pulmonary endothelial damage.
32
Which lung structures are most susceptible to oxygen toxicity?
Type I alveolar epithelial cells and capillary endothelium are highly vulnerable due to their thin barrier, high metabolic activity, and role in gas exchange.
33
What is absorptive atelectasis and how does high FiO₂ contribute?
High FiO₂ (>80–100%) reduces nitrogen content, leading to rapid gas resorption in poorly ventilated alveoli, promoting alveolar collapse and worsening V/Q mismatch.
34
Which cellular antioxidants normally mitigate oxygen toxicity?
Superoxide dismutase, catalase, and glutathione peroxidase are key antioxidants that detoxify ROS; their depletion contributes to lung injury in hyperoxia.
35
What are the five WHO functional classifications of pulmonary hypertension (PH)?
Group 1: Pulmonary arterial hypertension (PAH), Group 2: PH due to left heart disease, Group 3: PH due to lung disease/hypoxia, Group 4: PH due to thromboembolism, Group 5: Multifactorial/unknown mechanisms.
36
What is the mechanism of sildenafil in treating PH in dogs?
Sildenafil is a PDE-5 inhibitor that increases cGMP in pulmonary vascular smooth muscle, causing vasodilation and reduced pulmonary artery pressures.
37
What are the adverse effects of sildenafil in veterinary patients?
Common side effects include systemic hypotension, GI upset, and tachycardia; caution is needed in left-sided heart disease due to potential worsening of pulmonary edema.
38
How does pimobendan affect pulmonary hypertension pathophysiology?
Pimobendan acts as a positive inotrope and vasodilator (inodilator), enhancing contractility while reducing afterload in right heart failure secondary to PH.
39
What is the role of endothelin receptor antagonists in PH management (human medicine)?
Drugs like bosentan block vasoconstrictive and proliferative effects of endothelin-1 on pulmonary vasculature; not yet widely used in veterinary medicine but may have future potential.
40
How does species variation influence respiratory diagnostics?
Dogs are more tolerant of nasal catheter EtCO₂ monitoring; cats often require intubation or sedated blood gas sampling due to stress and anatomy. Species-specific anatomy and behavior affect technique feasibility.
41
What is a key difference in bronchial anatomy between dogs and cats?
Cats have more reactive airways and are predisposed to bronchoconstriction (e.g., asthma), whereas dogs more commonly suffer from bronchitis or tracheobronchomalacia.
42
Why is feline asthma considered a type I hypersensitivity disorder?
It involves IgE-mediated mast cell degranulation in response to inhaled allergens, resulting in bronchoconstriction, eosinophilic inflammation, and airway remodeling.
43
What role does bronchoalveolar lavage (BAL) play in species-specific diagnosis of respiratory disease?
BAL cytology in cats often shows eosinophilic or mixed inflammation in asthma; in dogs with bronchitis, neutrophilic inflammation predominates. BAL helps tailor antimicrobial vs anti-inflammatory therapy.
44
What respiratory diseases are unique or more common in brachycephalic breeds?
Brachycephalic obstructive airway syndrome (BOAS), dynamic laryngeal/pharyngeal collapse, and chronic hypoventilation with increased risk of hypercapnia.
45
What mechanical ventilation parameters should be modified for small-breed dogs or cats?
Use smaller tidal volumes (6–8 mL/kg ideal body weight), higher respiratory rates (16–24 brpm), shorter inspiratory times, and vigilant monitoring of airway pressure to prevent barotrauma.
46
Why must tidal volume be calculated using ideal body weight in ARDS ventilation?
Using actual body weight overestimates lung size, leading to volutrauma. Ideal body weight ensures lung-protective tidal volume delivery (~6 mL/kg).
47
Which ARDS patients benefit most from high PEEP strategies?
Patients with recruitable lung tissue (i.e., collapsed but aeratable alveoli) benefit from high PEEP to maintain alveolar recruitment and oxygenation.
48
What are the risks of high PEEP in ARDS management?
High PEEP can overdistend alveoli (volutrauma), reduce venous return (hypotension), and worsen V/Q mismatch in non-recruitable lungs.
49
Why is driving pressure considered a superior predictor of mortality in ARDS?
Driving pressure (Pplat – PEEP) reflects lung compliance; values <15 cm H₂O are associated with lower mortality and improved outcomes.
50
What is the purpose of recruitment maneuvers, and why are they used cautiously in veterinary medicine?
Recruitment maneuvers transiently open collapsed alveoli; however, they can cause barotrauma and hypotension, so use is limited in veterinary patients.
51
What is permissive hypercapnia, and when is it contraindicated?
Permissive hypercapnia allows higher PaCO₂ to minimize volutrauma. It is contraindicated in patients with increased ICP or serious arrhythmias.
52
What is the threshold FiO₂ and exposure time above which oxygen toxicity becomes a concern?
Oxygen toxicity occurs with FiO₂ >0.6 for longer than 12–24 hours, leading to oxidative damage in pulmonary tissues.
53
What is the primary pathophysiologic mechanism of oxygen toxicity?
Formation of reactive oxygen species (ROS) leads to lipid peroxidation, mitochondrial dysfunction, surfactant inhibition, and alveolar-capillary injury.
54
Which pulmonary cells are most vulnerable to oxygen toxicity?
Type I alveolar epithelial cells and pulmonary capillary endothelial cells are most susceptible due to their thin structure and high metabolic demands.
55
What is absorptive atelectasis and how is it caused by high FiO₂?
High FiO₂ reduces nitrogen levels, causing gas resorption from poorly ventilated alveoli, leading to alveolar collapse and V/Q mismatch.
56
Which antioxidant enzymes protect against oxygen toxicity?
Superoxide dismutase, catalase, and glutathione peroxidase neutralize ROS and help prevent cellular injury from hyperoxia.
57
Why should PaO₂ >120 mmHg be avoided during mechanical ventilation?
Hyperoxia at these levels increases oxidative stress, promotes vasoconstriction, and is associated with worse outcomes in ARDS patients.
58
What are the five WHO functional classifications of pulmonary hypertension?
Group 1: PAH, Group 2: Left heart disease, Group 3: Lung disease/hypoxia, Group 4: Thromboembolism, Group 5: Multifactorial/unknown.
59
What is the mechanism of sildenafil in canine PH?
Sildenafil inhibits phosphodiesterase-5 (PDE-5), increasing cGMP in pulmonary smooth muscle, leading to vasodilation and reduced pulmonary pressures.
60
What is a major risk when using sildenafil in dogs with left-sided heart disease?
Pulmonary vasodilation can worsen pulmonary edema by increasing pulmonary capillary hydrostatic pressure in dogs with elevated LA pressures.
61
How does pimobendan support dogs with PH?
Pimobendan increases myocardial contractility and causes vasodilation (inodilator), reducing RV afterload and improving cardiac output.
62
What is the role of endothelin receptor antagonists (e.g., bosentan) in PH?
These block endothelin-1's vasoconstrictive and proliferative effects, but are not yet widely available in veterinary medicine.
63
How does oxygen therapy itself act as a treatment for Group 3 PH?
Oxygen relieves hypoxic vasoconstriction, a primary driver of Group 3 PH due to chronic hypoxemia, improving pulmonary hemodynamics.
64
Why are nasal catheter EtCO₂ readings less reliable in cats than dogs?
Cats have smaller nares and are more prone to stress-induced hyperventilation, making sampling less consistent and accurate.
65
What is a key difference in feline and canine airway disease pathophysiology?
Feline asthma involves eosinophilic, reversible bronchoconstriction; canine bronchitis is neutrophilic, chronic, and often irreversible.
66
What mechanism underlies feline asthma as a type I hypersensitivity disorder?
Allergen exposure leads to IgE-mediated mast cell degranulation, bronchoconstriction, eosinophilic inflammation, and airway remodeling.
67
How does BAL cytology differ between feline asthma and canine bronchitis?
Feline asthma shows eosinophilic or mixed inflammation; canine bronchitis is typically neutrophilic with chronic changes.
68
Which respiratory disorders are more prevalent in brachycephalic dogs?
BOAS, pharyngeal/laryngeal collapse, tracheal hypoplasia, and chronic hypoventilation are common in brachycephalic breeds.
69
What is a common cause of post-extubation respiratory distress in brachycephalic dogs?
Pharyngeal collapse or laryngeal edema can lead to upper airway obstruction post-extubation; tracheostomy may be needed.
70
How should ventilator settings be adjusted in cats or small-breed dogs?
Use lower tidal volumes (6–8 mL/kg), higher respiratory rates, shorter inspiratory times, and monitor for barotrauma closely.
71
What does an increased PaCO₂–EtCO₂ gradient suggest in a ventilated patient?
It indicates increased dead space ventilation from causes like low cardiac output, overdistension, or pulmonary thromboembolism.
72
How can you differentiate ARDS from cardiogenic pulmonary edema on diagnostics?
ARDS: normal heart size, proteinaceous edema, poor furosemide response; CHF: cardiomegaly, perihilar edema, rapid diuretic response.
73
What does a "shark-fin" appearance on a capnograph waveform suggest?
A prolonged expiratory upstroke ("shark-fin") indicates bronchospasm, airway obstruction, or asthma—common in cats and brachycephalic dogs.
74
What waveform abnormality is seen with auto-PEEP (intrinsic PEEP)?
In flow-time graphs, expiratory flow fails to return to baseline before the next breath, indicating breath stacking and air trapping.
75
How can you differentiate compliance vs resistance issues on pressure-time waveforms?
High resistance = normal plateau pressure but high peak pressure; low compliance = elevated both peak and plateau pressures.
76
What does a 'scalloped' or 'concave' pressure-volume loop during inspiration indicate?
Patient-initiated effort (active inspiration) in pressure-controlled ventilation—common with inadequate sedation or dyssynchrony.
77
How does increased airway resistance affect the flow-volume loop?
It causes a "scooped out" expiratory curve with a prolonged return to baseline—seen in bronchoconstriction or tracheal collapse.
78
What ventilator change is recommended when intrinsic PEEP is identified?
Decrease respiratory rate or increase expiratory time (I:E ratio), and reduce tidal volume to prevent breath stacking.
79
What is the dose range of sildenafil in dogs for PH?
1–2 mg/kg PO q8–12h; adjust based on response and tolerance. Monitor for systemic hypotension and GI upset.
80
What is the typical dose of sildenafil in cats with pulmonary hypertension?
0.25–1 mg/kg PO q8–12h; start low and titrate. Clinical evidence is limited and off-label.
81
What is the starting dose of pimobendan for right heart failure or PH in dogs?
0.25–0.3 mg/kg PO q12h; off-label for PH but used in cases of right-sided CHF or cor pulmonale.
82
When should sildenafil be avoided in dogs?
In cases with moderate-to-severe left atrial enlargement or concurrent pulmonary edema, as pulmonary vasodilation can worsen hydrostatic pressure and fluid extravasation.
83
What was the main finding of the LOVS trial (2008) in ARDS patients?
The LOVS trial showed that a lung open ventilation strategy (high PEEP + recruitment maneuvers) did not reduce mortality compared to low PEEP.
84
What was the key result of the OSCILLATE trial (2013)?
High-frequency oscillatory ventilation (HFOV) increased mortality compared to conventional lung-protective ventilation in early ARDS.
85
What controversy did the ART trial (2017) uncover in ARDS management?
The ART trial showed that aggressive recruitment maneuvers and high PEEP strategies increased 28-day mortality, suggesting harm from overaggressive lung opening.
86
What board-relevant conclusion can be drawn from ART and OSCILLATE trials?
Lung-protective ventilation (low tidal volume + moderate PEEP) remains superior; overaggressive PEEP or recruitment increases harm.
87
How did the EXPRESS trial (2008) inform PEEP titration?
Targeting PEEP to achieve a plateau pressure of 28–30 cm H₂O improved oxygenation but did not improve mortality.
88
What is the currently recommended approach to PEEP titration in ARDS?
Use moderate PEEP tailored to individual compliance and oxygenation needs; avoid excessive recruitment maneuvers unless hypoxemia is refractory.
89
What is the general board-prep rule for ARDS tidal volume settings?
Use 4–6 mL/kg ideal body weight to minimize volutrauma; accept permissive hypercapnia if pH remains >7.2.
90
Which ventilator parameters are considered 'lung-protective' in ARDS?
Low tidal volume (4–6 mL/kg IBW), plateau pressure <30 cm H₂O, driving pressure <15 cm H₂O, moderate PEEP, and permissive hypercapnia.
91
What trial showed that hyperoxia can be harmful in ARDS?
The 2018 trial by Aggarwal et al. showed PaO₂ >80 mmHg was associated with worse outcomes in ARDS, highlighting the risks of hyperoxia.
92
What oxygen target is considered safe in mechanically ventilated patients?
Target PaO₂ 60–80 mmHg (SpO₂ 90–97%) to avoid both hypoxia and hyperoxia.

ACVECC Top 100(?) Papers (11 decks)

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